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sábado, 16 de abril de 2022

Científicos desconcertados buscan la causa de un extraño y alarmante brote de hepatitis grave en niños pequeños

 

 Los médicos de los principales centros hepáticos pediátricos de los Países Bajos y Dinamarca dijeron ayer a Science Insider que están viendo tendencias similares. "Hay niños que están muy enfermos y han sido remitidos para un trasplante".

https://twitter.com/jturnesv/status/1525938723430490112

Mysterious hepatitis outbreak sickens young children in Europe as CDC probes

Los investigadores sospechan que puede tratarse de un adenovirus, pero siguen buscando la causa de la enfermedad


Científicos desconcertados buscan la causa de un extraño y alarmante brote de hepatitis grave en niños pequeños, con 74 casos documentados en el Reino Unido y tres en España. Los médicos de Dinamarca y los Países Bajos también informan de casos similares. Y en Estados Unidos, los Centros para el Control y la Prevención de Enfermedades (CDC) dijeron a última hora de ayer que están investigando nueve casos en Alabama.


Los virus pueden causar hepatitis, una inflamación del hígado, pero los niños por lo demás sanos rara vez enferman gravemente. Hasta el 12 de abril, ninguno de los niños del Reino Unido o de España ha muerto, pero algunos están muy enfermos: Todos han sido ingresados en hospitales y siete han necesitado trasplantes de hígado, seis de ellos en el Reino Unido, según un comunicado de la Organización Mundial de la Salud (OMS) publicado hoy. Dos de los nueve niños afectados en Alabama han necesitado trasplantes de hígado, según ha anunciado esta tarde el Departamento de Salud Pública del estado.


La principal teoría es que el culpable es un adenovirus, una familia de virus que suele causar resfriados; hasta la mitad de los niños enfermos en el Reino Unido dieron positivo en un virus de este tipo, al igual que todos los niños de Alabama. Pero hasta ahora, las pruebas son demasiado escasas para resolver el misterio, dicen los investigadores y los médicos.


"Se trata de un fenómeno grave", afirma Deirdre Kelly, hepatóloga pediátrica del Hospital Infantil de Birmingham, en Inglaterra. "Estos [eran] niños perfectamente sanos... hasta hace una semana". Sin embargo, no todas las noticias son malas. "La mayoría [de los niños] se recuperan por sí mismos", señala Kelly.


"Esto debe tomarse en serio", dijo la Oficina Regional de la OMS para Europa en un comunicado enviado por correo electrónico. "El aumento es inesperado y se han excluido las causas habituales".


Los investigadores escoceses identificaron por primera vez el brote el 31 de marzo, cuando alertaron a Salud Pública de Escocia de un grupo de niños de entre 3 y 5 años ingresados en el Royal Hospital for Children de Glasgow en las tres primeras semanas de marzo. A todos ellos se les diagnosticó una hepatitis grave de causa desconocida. Por lo general, en Escocia se dan menos de cuatro casos de este tipo al año, escribieron los investigadores en un artículo publicado ayer. Pero hasta el 12 de abril se habían producido 13 casos en niños escoceses, todos menos uno en marzo y abril.
 

Researchers suspect an adenovirus may be involved, but are still searching for the cause of illness

Puzzled scientists are searching for the cause of a strange and alarming outbreak of severe hepatitis in young children, with 74 cases documented in the United Kingdom and three in Spain. Clinicians in Denmark and the Netherlands are also reporting similar cases. And in the United States, the Centers for Disease Control and Prevention (CDC) said late yesterday it is investigating nine cases in Alabama.

Viruses can cause hepatitis, an inflammation of the liver, but otherwise-healthy children rarely become seriously ill. As of 12 April, none of the U.K. or Spanish children have died, but some are very sick: All have been admitted to hospitals and seven required liver transplants, six of them in the United Kingdom, according to a World Health Organization (WHO) statement issued today. Two of the nine affected children in Alabama have required liver transplants, the state’s Department of Public Health announced this afternoon.

The leading theory is that an adenovirus, a family of viruses that more typically cause colds, is the culprit—up to half of the sickened children in the United Kingdom tested positive for such a virus, as did all the children in Alabama. But so far, the evidence is too thin to resolve the mystery, researchers and physicians say.

“This is a severe phenomenon,” says Deirdre Kelly, a pediatric hepatologist at Birmingham Children’s Hospital in England. “These [were] perfectly healthy children … up to a week ago.” Not all the news is bad, however. “Most of [the children] recover on their own,” Kelly notes.

“This should be taken seriously,” WHO’s Regional Office for Europe said in an emailed statement. “The increase is unexpected and the usual causes have been excluded.”

Scottish investigators first identified the outbreak on 31 March, when they alerted Public Health Scotland to a cluster of 3- to-5-year-olds admitted to the Royal Hospital for Children in Glasgow in the first 3 weeks of March. Each was diagnosed with severe hepatitis of unknown cause. Typically, Scotland sees fewer than four such cases annually, the investigators wrote in a paper published yesterday. But there have been 13 cases in Scottish children as of 12 April, all but one in March and April.

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Kelly, que trabaja en uno de los tres centros de Inglaterra para enfermedades hepáticas pediátricas y trasplantes, dice que desde el comienzo de este año, su unidad ha visto 40 casos de hepatitis infantil de causa incierta. En el mismo período de enero a abril de 2018, su unidad vio solo siete niños de este tipo.

La mayoría de los niños del Reino Unido tienen entre 2 y 5 años, según un comunicado emitido el 8 de abril por la Agencia de Seguridad Sanitaria del Reino Unido. El Centro Europeo para la Prevención y el Control de Enfermedades emitió una alerta pública el 12 de abril sobre el brote del Reino Unido, señalando que los vómitos y la ictericia -amarilleo de la piel y el blanco de los ojos- son síntomas comunes.

Las primeras hipótesis sobre lo que podría estar enfermando a los niños incluían una exposición tóxica a través de los alimentos, las bebidas o los juguetes, pero las sospechas se centran ahora en un virus. Ninguno de los niños del Reino Unido o de España tenía los virus de la hepatitis A, B, C o E, causas infecciosas típicas de la enfermedad. Sin embargo, un puñado de niños dio positivo en la prueba de infección por SARS-CoV-2 poco antes o en el momento del ingreso en el hospital; ninguno había recibido la vacuna COVID-19. Además, hasta la mitad tenía adenovirus, un virus común que se transmite por gotitas respiratorias y por tocar a personas infectadas o virus en superficies. Puede provocar vómitos, diarrea, conjuntivitis y síntomas de resfriado, pero rara vez causa hepatitis.

"Las principales hipótesis se centran en el adenovirus, ya sea una nueva variante con un síndrome clínico distinto o una variante que circula habitualmente y que está afectando más gravemente a los niños más pequeños que son inmunológicamente ingenuos", escribieron los investigadores escoceses.

El aislamiento de los niños más pequeños durante el cierre de la pandemia puede haberlos dejado inmunológicamente vulnerables porque no han estado expuestos a la multiplicidad de virus, incluidos los adenovirus, que suelen acompañar a los niños pequeños. "Estamos viendo un aumento de las infecciones víricas típicas de la infancia cuando los niños salen del bloqueo, [así como] un aumento de las infecciones por adenovirus", pero no podemos estar seguros de que una sea la causa de la otra, dice Will Irving, virólogo clínico de la Universidad de Nottingham.

Los investigadores siguen estudiando otras posibilidades. Por ejemplo, los efectos inmunológicos de un episodio anterior de COVID-19 podrían haber dejado a los niños más vulnerables a la infección o la enfermedad podría ser una complicación a largo plazo de la propia COVID-19. Tampoco se ha descartado una toxina no identificada.

Todos los casos podrían no tener una única causa, advierte Jim McMenamin, epidemiólogo que dirige el servicio de infecciones de Public Health Scotland. "Es muy importante que nos aseguremos de buscar todo, que no nos limitemos a decir que se trata simplemente de una causa viral".

En Estados Unidos, los CDC están ayudando al Departamento de Salud Pública de Alabama a investigar nueve casos de hepatitis en niños con edades comprendidas entre 1 y 6 años y que también dieron positivo en las pruebas de adenovirus. Los casos se han producido desde octubre de 2021, dijo Kristen Nordlund, portavoz de los CDC, en el comunicado enviado por correo electrónico a ScienceInsider anoche.

"Los CDC están trabajando con los departamentos de salud estatales para ver si hay casos adicionales en los Estados Unidos, y qué puede estar causando estos casos", escribió. "El adenovirus puede ser la causa de estos, pero los investigadores todavía están aprendiendo más, incluyendo el descarte de las causas más comunes de la hepatitis".

Wes Stubblefield, funcionario médico del Departamento de Salud Pública de Alabama, dijo hoy en una entrevista que el caso más reciente en Alabama se produjo en febrero, y que cinco de los nueve niños dieron positivo para el adenovirus-41, una cepa que suele causar gastroenteritis.

Mientras tanto, en España, el gobierno de la Comunidad de Madrid anunció el 13 de abril que tres regiones -Madrid, Aragón y Castilla-La Mancha- habían notificado cada una un caso de hepatitis grave de origen desconocido en niños pequeños. Un niño ha recibido un trasplante de hígado.

Los médicos de los principales centros hepáticos pediátricos de los Países Bajos y Dinamarca dijeron ayer a ScienceInsider que están observando tendencias similares. "Hay niños que están muy enfermos y que han sido remitidos para un trasplante, dice Ruben de Kleine, cirujano de trasplantes hepáticos pediátricos del Centro Médico Universitario de Groningen. "Hemos evaluado un número similar de niños para trasplante en los primeros 4 meses de 2022 [al que hacemos] normalmente en todo un año".

También en el Hospital Universitario de Copenhague "tenemos más casos con [insuficiencia hepática aguda] de los que normalmente tenemos", dice la hepatóloga pediátrica Marianne Hørby Jørgensen. Ningún niño ha necesitado un trasplante.

Tanto Hørby Jørgensen como de Kleine subrayan que los padres no deben entrar en pánico. Hasta la fecha, los médicos han identificado un pequeño número de casos en sus países, donde, en conjunto, nacen más de 230.000 niños al año.


Kelly, who works at one of England’s three centers for pediatric liver disease and transplantation, says that since the start of this year, her unit has seen 40 cases of childhood hepatitis of uncertain cause. Over the same January to April period in 2018, her unit saw only seven such children.

Most of the U.K. children are 2 to 5 years old, according to a statement issued on 8 April by the UK Health Security Agency. The European Centre for Disease Prevention and Control issued a public alert on 12 April about the U.K. outbreak, noting that vomiting and jaundice–yellowing of the skin and the whites of the eyes—are common symptoms.

Early hypotheses about what might be making the children sick included a toxic exposure from food, drinks, or toys, but suspicion now centers on a virus. None of the U.K. or Spanish kids had the hepatitis A, B, C, or E viruses, typical infectious causes of the disease. But a handful of children tested positive for SARS-CoV-2 infection shortly before or upon hospital admission; none had received a COVID-19 vaccine. In addition, as many as half had adenovirus, a common virus passed by respiratory droplets and from touching infected people or virus on surfaces. It can cause vomiting, diarrhea, conjunctivitis, and cold symptoms but rarely causes hepatitis.

“The leading hypotheses center around adenovirus—either a new variant with a distinct clinical syndrome or a routinely circulating variant that is more severely impacting younger children who are immunologically naïve,” the Scottish investigators wrote.

Isolation of the youngest children during the pandemic lockdown may have left them immunologically vulnerable because they haven’t been exposed to the multiplicity of viruses, including adenoviruses, that typically attend toddlerhood. “We are seeing a surge in typical childhood viral infections as children come out of lockdown, [as well as] a surge in adenovirus infections”—but can’t be sure that one is causing the other, says Will Irving, a clinical virologist at the University of Nottingham.

Researchers continue to study other possibilities. For example, the immunological effects of a prior episode of COVID-19 might have left children more vulnerable to infection or the illness could be a long-term complication of COVID-19 itself. An unidentified toxin has also not been ruled out.

All the cases might not have a single cause, cautions Jim McMenamin, an epidemiologist who heads the infection service of Public Health Scotland. “It’s awfully important that we ensure we are looking for everything, that we are not confining ourselves to saying this is simply one viral cause.”

In the United States, CDC is helping the Alabama Department of Public Health investigate nine cases of hepatitis in children ranging in age from 1 to 6 years old and who also tested positive for adenovirus. The cases have occurred since October 2021, Kristen Nordlund, a CDC spokesperson, said in the statement emailed to ScienceInsider last night. 

“CDC is working with state health departments to see if there are additional U.S. cases, and what may be causing these cases,” she wrote. “Adenovirus may be the cause for these, but investigators are still learning more—including ruling out the more common causes of hepatitis.”

Wes Stubblefield, a medical officer with the Alabama Department of Public Health, said in an interview today that the most recent case in Alabama occurred in February, and that five of the nine children tested positive for adenovirus-41, a strain that commonly causes gastroenteritis.

Meanwhile, in Spain, the government of the Madrid region announced on 13 April that three regions—Madrid, Aragón, and Castilla-La Mancha—had each reported a case of severe hepatitis of unknown origin in young children. One child has received a liver transplant.

Physicians at major pediatric liver centers in the Netherlands and Denmark told ScienceInsider yesterday they are seeing similar trends. “There are children that are very sick and have been referred for transplantation, says Ruben de Kleine, a pediatric liver transplant surgeon at University Medical Center Groningen. “We have assessed a similar number of kids for transplantation within the first 4 months of 2022 [to what we] normally do in a whole year.”

At Copenhagen University Hospital, too, “we have more cases with [acute liver failure] than we normally have,” says pediatric hepatologist Marianne Hørby Jørgensen. No children there have needed transplants.

Hørby Jørgensen and de Kleine both stress that parents should not panic. To date, clinicians have identified small numbers of cases in their countries where, combined, more than 230,000 infants are born each year.

Update, 15 April, 3:00 p.m.: This story has been updated to include more details about the Alabama cases.

 

 

https://www.science.org/content/article/mysterious-hepatitis-outbreak-sickens-young-children-europe-cdc-probes-cases-alabama#.YlnShCcbklo.twitter

Detectados en España tres casos de una hepatitis infantil de origen desconocido

Los diagnósticos se producen tras una alerta internacional de la OMS y el ECDC iniciada en el Reino Unido, que ha atendido en sus hospitales a 74 niños. Uno de los menores españoles y seis británicos han necesitado un trasplante de hígado 

España ha detectado los tres primeros casos de una forma de hepatitis aguda de origen desconocido que afecta a niños menores de 10 años.

Europa vuelve a estar en alerta por una amenaza infecciosa y esta vez no es ningún coronavirus. El Reino Unido ha puesto sobre aviso a la UE tras detectar un brote inusual de una hepatitis de origen desconocido en niños y adolescentes. La sanidad británica investiga más de 70 afectados que desarrollaron la enfermedad. La mayoría tienen entre dos y cinco años, algunos no necesitaron tratamiento, pero en un pequeño número de casos la evolución fue tan mala que desencadenó un fallo hepático y necesitaron un trasplante de hígado para sobrevivir.

Reino Unido compartió su preocupación con la Organización Mundial de la Salud y el ECDC, el centro europeo que monitoriza las enfermedades, para averiguar si en otros países existían brotes similares.

Desde el pasado lunes, España y otros países de la UE están revisando sus historiales para rastrear hepatitis de origen desconocido. De momento, solo la Comunidad de Madrid ha notificado tres casos aislados, sin conexión entre ellos, que han sido tratados en el Hospital La Paz.

Los pacientes españoles tienen edades comprendidas entre los dos y los siete años y proceden de Madrid, Aragón y Castilla-La Mancha. Solo uno de ellos sufrió la evolución más grave y necesitó un trasplante de hígado, según ha informado la Consejería de Sanidad. Los pacientes se trasladaron al hospital madrileño, precisamente, por tratarse de un centro de referencia en trasplante hepático infantil.

Buena evolución

Los tres niños evolucionaron favorablemente y ya no están hospitalizados. Sus casos han salido a la luz después de que los servicios de Salud Pública iniciaran la búsqueda de casos similares a los del Reino Unido. El Ministerio de Sanidad pidió a las comunidades autónomas y a las sociedades científicas de Pediatría y gerencias de hospitales una «observación y búsqueda activa» de posibles casos infantiles de esta misteriosa hepatitis. Ese rastreo no empieza ahora, se ha pedido que se revisen las historias clínicas desde comienzo de año que coincidan con el reporte del Reino Unido.

Pablo Rojo: «No es la primera vez que se diagnostican hepatitis agudas no filiadas, es decir de origen desconocido»

Se buscan hepatitis agudas cuyo origen no es ninguno de los virus conocidos que causan la enfermedad. Es decir no son A, B, C, D ni E. Tampoco se han relacionado con otros virus conocidos como el citomegalovirus o el Epstein-Barr que también puede estar relacionado con la enfermedad. Ni consumieron una dosis tóxica de paracetamol, un fármaco que en dosis elevadas puede producir fallo hepático. «Suele ser relativamente frecuente el caso de niños que toman accidentalmente el famoso apiretal», cuenta Pablo Rojo, pediatra y especialista en enfermedades infecciosas del Hospital 12 de Octubre de Madrid.

Sin vínculo con el Covid

Las autoridades sanitarias sospechan de un origen vírico aún sin identificar. Pero este especialista llama a la calma: «No es un hecho nuevo que se diagnostiquen hepatitis agudas no filiadas, es decir de origen desconocido. Si son casos aislados no deberíamos inquietarnos. Lo importante del brote del Reino Unido es la agrupación de casos. Debemos estar alerta, pero es muy pronto para saber si estamos ante una situación preocupante y lo que sabemos es solo la punta del iceberg. Si el Reino Unido ha sido el primero en notificarlo puede ser simplemente porque tienen un sistema muy ágil de vigilancia», explica.

Las primeras investigaciones ya han descartado que la enfermedad esté relacionada con la vacunación del Covid ni con el propio coronavirus. No todos los niños afectados habían pasado el virus pandémico. La conclusión de las autoridades británicas es que, hasta el momento, no hay una conexión clara entre los casos, ni asociación tampoco con algún viaje a otro país. La mayoría de los niños enfermos están en Inglaterra (60) y en Escocia (10). En Gales, actualmente no se conocen casos bajo investigación, pero un número muy pequeño de casos de principios de 2022 tuvo presentaciones clínicas similares. En Irlanda del Norte, no hay actualmente ningún caso confirmado, según el ECDC.

Sí comparten síntomas: dolor abdominal, vómitos o ictericia (coloración amarillenta de la piel). Se detecta con una analítica sencilla. Basta con hacer un análisis de sangre para detectar niveles muy altos de transaminasas, las enzimas que indican un daño hepático.

La evolución suele ser buena, aunque algunos casos se produce fallo hepático y es necesario hacer un trasplante de hígado

La evolución de los afectados es imprevisible y para estos casos no existe un tratamiento específico porque no se identifica la causa. «Por ejemplo, los fármacos que funcionan para la hepatitis C no estarían indicados. En esta situación, se proporciona una terapia de soporte. A veces es necesario aportar plasma si desencadena una alteración de la coagulación. Y en la situación más grave, cuando se produce un fallo hepático solo cabe hacer un trasplante de hígado para salvar la vida del paciente. Estos trasplantes tienen una urgencia cero, deben hacerse lo más rápido posible», cuenta el experto en infecciones pediátricas.

Origen zoonótico

El brote que inquieta en Europa afecta a menores de 16 años, aunque las hepatitis de origen desconocido también pueden afectar a adultos y las causas son muy variadas. Recientemente, investigadores españoles han descrito los primeros casos de hepatitis aguda en Europa provocados por un nuevo virus de origen zoonótico, el Orthohepevirus C, lo que puede suponer una nueva causa emergente de hepatitis aguda en Europa debido a la prevalencia detectada entre pacientes con hepatitis aguda de origen desconocido.

El principal reservorio animal de este virus son los roedores, sin embargo, ninguno de los casos identificados en el estudio refería haber tenido contacto directo con ellos. Estos resultados sugieren la existencia de una vía de transmisión animal-humano aun no identificada y que por tanto requiere ser evaluada.

https://www.abc.es/sociedad/abci-espana-rastrea-hepatitis-origen-desconocido-ninos-desde-enero-202204140022_noticia.html 

Sobre la hepatitis de origen desconocido. Reportados 190 casos en Europa, Reino Unido, Israel y EEUU. Se baraja sea un adenovirus. ¿Ha sufrido algún tipo de mutación?¿Tiene algo que ver el SARSCoV2?


Global health officials probe unexplained child hepatitis cases

The mystery illness has been recorded in the US, Israel and 10 EU countries

The mystery illness has been recorded in the US, Israel and 10 EU countries Hepatitis A virus that is almost always benign (picornavirus) 

The viruses that commonly caused acute viral hepatitis had not been detected in any of the cases reported in children around the world, said the WHO’s director-general © BSIP/Universal Images Group/Getty Images Share on twitter (opens new window) Share on facebook (opens new window) Share on linkedin (opens new window) Oliver Barnes and Sarah Neville in London April 26 2022 10 Print this page Receive free Disease control and prevention updates We’ll send you a myFT Daily Digest email rounding up the latest Disease control and prevention news every morning. Global health authorities are investigating unexplained severe hepatitis cases in children that have been recorded in more than a dozen countries worldwide. About 190 cases of severe liver inflammation of unknown origin had been identified around the world, the European Centre for Disease Prevention and Control said on Tuesday. British health officials first sounded the alarm about the mysterious illness, which has largely affected children aged under 10 years old, in early April. Andrea Ammon, ECDC director, said investigations about what lay behind the outbreak were “ongoing” but “the exact cause of this hepatitis still remains unknown”. She said early findings “point towards a link to adenovirus infection”. Adenovirus — a group of viruses typically associated with symptoms, such as a persistent cough, conjunctivitis or diarrhoea — rarely leads to hepatitis in healthy children. One possible factor, said Ammon, was that children having “little exposure” to adenovirus as a result of decreased social mixing because of Covid-19 restrictions was contributing to more severe outcomes.

 However, she cautioned that in terms of explaining why the cases were emerging now: “it’s all speculation”.

 Three-quarters of the British children who were tested for adenovirus after falling ill with the unexplained hepatitis returned positive results, according to data from the UK Health Security Agency published on Monday. The UK had recorded 111 cases of the illness, as of April 21. The US, Israel and 10 other European nations have also recorded cases. Tedros Adhanom Ghebreyesus, the World Health Organization’s director-general, told a news conference that 17 children had required liver transplants and one had child died after contracting the illness. He said symptoms included abdominal pain, diarrhoea, vomiting, jaundice, severe acute hepatitis, and increased levels of liver enzymes. However, the viruses that commonly caused acute viral hepatitis had not been detected in any of the cases. Adenovirus had been detected in at least 74 cases and this, and other hypotheses, were being explored, Tedros said. The WHO was “working closely with the European Centre for Disease Prevention and Control and the affected countries to support ongoing investigations, including additional lab testing”, he added. Scientists are also investigating whether adenovirus combined with previous coronavirus infection or simultaneous Covid-19 infection could be behind the increase in severe hepatitis. Genomic sequencing analysis is under way to determine whether the adenovirus type 41, which has been linked to the outbreak, has taken on mutations which could lead to hepatitis. But health officials have ruled out the possibility that traditional types of hepatitis viruses — A to E — are the cause of the outbreak, or that Covid-19 vaccination is to blame. Phillippa Easterbrook, a medical expert in the WHO’s HIV, hepatitis and sexually transmitted infection programme, added that it was “very unusual for an adenovirus to cause this type of severe symptoms”. She said reports of unexplained hepatitis in children occurred every year and it was possible that increased testing and awareness might be “flushing out and recognising more cases that have always existed”.

https://www.ft.com/content/bf382b57-0550-4f2d-b6e7-c35bb26575d9

 

viernes, 8 de abril de 2022

Sistema inmunitario humano y evolución de los virus

 

Sistema inmunitario humano y evolución de los virus

Una investigación reciente ha explorado hasta qué punto el sistema inmunitario humano puede influir en la evolución de los virus.

 Durante la pandemia de la COVID-19, algunas personas se han infectado varias veces con el virus SARS-CoV-2 mientras que otras no lo han hecho nunca. La susceptibilidad a la infección ante un virus tiene unas bases genéticas, pero, ¿la evolución del virus depende también de la genética del hospedador?

 Esta es la pregunta que guía una investigación realizada por el Instituto de Biología Integrativa de Sistemas (I2SysBio), centro mixto del Consejo Superior de Investigaciones Científicas (CSIC) y la Universidad de Valencia (UV), en España. Sus resultados sugieren que es el sistema inmunitario en su conjunto, y no las defensas específicas de forma aislada, quien restringe la diversidad y evolución viral.

 Este estudio, realizado en colaboración con el grupo de Carla Saleh del Instituto Pasteur de París en Francia, supone una mejora en la comprensión de cómo diferencias genéticas en poblaciones de hospedadores, en cuanto a resistencia a la infección, afectan a la evolución de la virulencia de los patógenos virales.

 “En primer lugar, hemos observado cómo el virus optimizaba su capacidad de reproducirse e infectar al genotipo del hospedador en el que estaba evolucionando de una manera altamente específica, dependiendo de la ruta de señalización y de la respuesta a la infección afectada en cada caso”, explica Santiago F. Elena, científico del CSIC que dirige el grupo de Virología Evolutiva y de Sistemas del I2SysBio. “Además, vimos que la adaptación al hospedador ocurría con una disminución de la virulencia, lo que sugiere que hospedadores inmunodeprimidos ejercen una presión de selección débil sobre las poblaciones virales, permitiendo que variantes del virus poco agresivas puedan persistir en la población”, continúa.

 

[Img #66044]

Partículas víricas, capaces de provocar gastroenteritis. (Imagen: Dr. Erskine Palmer / CDC)

 

Para realizar este estudio, los investigadores emplearon un modelo experimental formado por la mosca del vinagre (Drosophila melanogaster) y un virus que es uno de sus patógenos naturales. Empleando una colección de genotipos de la mosca con mutaciones en distintas rutas de señalización y respuesta a la infección, el equipo de investigación elaboró un experimento de evolución del virus, caracterizando la virulencia, el proceso por el que se desarrolla la enfermedad (patogénesis) y la variabilidad genética de los virus resultantes. También estudiaron qué fuerzas evolutivas (mutación, selección natural y azar) rigen la evolución del virus en cada genotipo de la mosca.

 Por último, el equipo de investigación observó que la cantidad de variabilidad genética acumulada por las poblaciones del virus, así como las mutaciones que acumulaba el virus en su genoma, dependían del genotipo preciso del huésped. “Globalmente, nuestros resultados indican que es el sistema inmunitario innato en su conjunto, y no las rutas de señalización y defensa específicas de forma aislada, quien restringe la diversidad y evolución viral”, resume Santiago Elena.

 ¿Este hallazgo tiene consecuencias para los tratamientos antivirales? Según el investigador del CSIC, los fármacos antivirales actúan sobre el propio virus o sobre su interacción con las células (bloqueando su entrada, por ejemplo), no sobre el sistema inmune. “Nuestro sistema inmune tiene dos componentes, el innato y el adaptativo. Lo que hemos estudiado aquí son las rutas innatas más importantes en invertebrados. Nuestro sistema adaptativo con memoria se estimula con infecciones naturales y, como es bien sabido, con las vacunas”.

 Los resultados permitirán desarrollar modelos más precisos sobre cómo los virus pueden evolucionar en poblaciones genéticamente heterogéneas, con niveles de inmunidad que varían con la edad y el estado nutricional, entre otros factores.

 El estudio se titula “Innate immune pathways act synergistically to constrain RNA virus evolution in Drosophila melanogaster”. Y se ha publicado en la revista académica Nature Ecology and Evolution.

 (Fuente: CSIC)

https://www.youtube.com/watch?v=aUHd114bs0g&feature=emb_imp_woyt 

 


Seguimiento del inmunofenotipado a los pacientes vacunados




 Componente principal del sistema inmunitario y en donde se lleva a cabo la mayor parte de "la acción" en la defensa contra los invasores.
 
 
 

 
 
 
Parches de Peyer (verde), micrografía electrónica de barrido de color (SEM), coloreada. Estas regiones de tejido linfoide se encuentran en el intestino humano.

Vacunas contra diversos cánceres con las mismas tecnologías de ARNm, ADN, vectores virales o proteínas.

  Vacunas contra diversos cánceres con las mismas tecnologías de ARNm, ADN, vectores virales o proteínas.

Una nueva generación de vacunas para prevenir el cáncer podría acabar con los tumores antes de que se formen

 

Las vacunas entran en los primeros ensayos clínicos para personas sanas con alto riesgo de padecer la enfermedad

Cuando Dave Dubin se enteró a los 29 años de que tenía cáncer de colon, no fue una gran sorpresa. Su abuelo y su padre habían sobrevivido a la enfermedad. "Era casi el estilo Dubin, y simplemente seguimos adelante", dice Dubin. Se sometió a cirugía y quimioterapia, pero el cáncer volvió a aparecer 10 años después. Las pruebas genéticas encontraron finalmente una explicación a las pruebas de su familia: una mutación en un gen de reparación del ADN que permite que los errores genéticos se acumulen en las células en división. La enfermedad, el síndrome de Lynch, conlleva hasta un 70% de riesgo de cáncer a lo largo de la vida.



Dubin, 55, gets annual colonoscopies, endoscopies, and imaging scans, which caught a third cancer, in his kidney. His eldest son, Zach Dubin, 26, inherited the DNA repair mutation and also regularly gets checked for cancer. “It’s no fun. Nobody enjoys it,” Dave Dubin says—not the 2-day colonoscopy prep and procedure, nor the worrying about possible tumors. The disease also turned him into an activist. He and his family in Haworth, New Jersey, launched a nonprofit, AliveAndKickn, to promote research and awareness of Lynch syndrome, which affects an estimated 1.1 million people in the United States.

“There is a lot of anxiety in this patient population,” says oncologist and geneticist Eduardo Vilar-Sanchez of the MD Anderson Cancer Center. “It is a big psychological burden.” In hopes of easing that strain, Vilar-Sanchez will soon lead a clinical trial of a vaccine to prevent or at least delay Lynch-related cancers. If it works, Dave Dubin says, “it could be huge.”

Ya existen vacunas para prevenir ciertos tipos de cáncer. Se dirigen a los virus: el virus de la hepatitis B, que puede provocar cáncer de hígado, y el virus del papiloma humano, que causa el cáncer de cuello de útero y algunos otros. Pero la mayoría de los cánceres no están causados por virus. El ensayo de la vacuna de Lynch será uno de los primeros ensayos clínicos de una vacuna para prevenir cánceres no virales.

La idea es introducir en el cuerpo trozos de proteínas, o antígenos, de las células cancerosas para estimular al sistema inmunitario a atacar cualquier tumor incipiente. El concepto no es nuevo, y se ha enfrentado al escepticismo. Hace una década, un editorial de Nature desestimó el objetivo de un destacado grupo de defensa del cáncer de mama de desarrollar una vacuna preventiva para 2020 por considerarlo "erróneo", en parte debido a la complejidad genética de los tumores. El editorial calificaba la meta como un "objetivo que la ciencia aún no puede cumplir". Pero ahora, algunos equipos -entre ellos uno financiado por el mismo grupo de defensa, la Coalición Nacional contra el Cáncer de Mama (NBCC)- están preparados para probar vacunas preventivas, en algunos casos en personas sanas con alto riesgo genético de padecer cáncer de mama y otros. Sus esfuerzos se han visto impulsados por los nuevos conocimientos sobre los cambios genéticos en los cánceres tempranos, junto con el reconocimiento de que, dado que incluso los tumores incipientes pueden suprimir el sistema inmunitario, las vacunas deberían funcionar mejor en personas sanas que nunca han tenido cáncer.

Traducción realizada con la versión gratuita del traductor www.DeepL.com/Translator
Antigen-presenting cells (APCs) take up antigen and display fragments on their surfaces. B cells and T cells recognize the antigen and produce antibodies and killer T cells. Person is healthy but at high risk of cancer. Vaccines using a tumor antigen can be viral, messenger RNA, DNA, or peptide-based. Healthy cell Cancer cell Intercepting cancers Preventive cancer vaccines deliver proteins known as tumor antigens, which are scarce on healthy cells but abundant on tumors, or neoantigens, which are unique to tumors. Immune cells take up the antigens and produce antibodies and killer T cells that attack incipient tumor cells, preventing cancer growth. B cell T cell Tumor-associated antigens or neoantigens APC Killer T cell Antibodies If tumor cells bearing the antigen develop, corresponding antibodies signal the immune system to destroy the cells. Killer T cells that recognize the antigen also attack cancer cells.
V. Altounian/Science

Researchers are trying out several vaccine strategies. Some use so-called tumor antigens, molecular markers that are scarce on healthy cells but plentiful on cancer cells. The Lynch vaccine instead targets “neoantigens,” a potent type of antigen only found on tumor cells. Some deploy just a single antigen whereas others use a large number, in a bid to broadly shield against cancer. The best approach is unclear, and developers also face the difficult challenge of measuring success without waiting decades for healthy people to develop cancers.

Early trials are yielding glimmers of promise. If the idea works to prevent one or a few cancers, it could be extended to meet an ambitious goal suggested by President Joe Biden: developing a vaccine that could prevent many types of cancer, modeled on the messenger RNA (mRNA) vaccines that have helped fight the COVID-19 pandemic. “We are a long way from a general vaccine” to prevent cancer, says medical oncologist Shizuko Sei of the National Cancer Institute’s Division of Cancer Prevention. “But it could be in the distant future. It’s a stepwise approach.”

Los esfuerzos por aprovechar el sistema inmunitario para combatir el cáncer tienen una larga historia. En la década de 1890, el médico William Coley informó de que las inyecciones de toxinas bacterianas -una especie de vacuna- a veces reducían los tumores de los pacientes, aparentemente estimulando el sistema inmunitario. Décadas más tarde, los investigadores descubrieron que las células inmunitarias llamadas células T podían reconocer los antígenos tumorales como extraños y atacar los cánceres. Este hallazgo dio lugar a dos clases de terapias aprobadas: fármacos que levantan los frenos moleculares de las células T para que puedan intensificar su ataque contra el cáncer, y células T diseñadas para atacar a las células cancerosas. Ambos tipos de tratamiento han tenido un éxito sorprendente contra ciertos tipos de cáncer.

Un tercer tipo de inmunoterapia, las vacunas para tratar el cáncer, se ha quedado atrás. Los esfuerzos despegaron a principios de la década de 1990, cuando los investigadores empezaron a contabilizar docenas de antígenos tumorales que podrían despertar las defensas inmunitarias de un paciente. A menudo estos antígenos son proteínas que las células cancerosas utilizan para crecer o propagarse, por lo que los antígenos son buenos marcadores de las células cancerosas.

Pero, a pesar de los datos prometedores de los experimentos con animales, la mayoría de las vacunas terapéuticas no han conseguido detener el crecimiento del tumor en las personas. Como los antígenos asociados a los tumores también pueden estar presentes en cantidades escasas en las células normales, el sistema inmunitario tiende a ignorarlos. La quimioterapia u otros tratamientos agresivos que reciben los pacientes con cáncer también debilitan su respuesta inmunitaria, y los tumores están protegidos por su "microambiente", es decir, células y moléculas circundantes que suprimen las células T asesinas y les impiden entrar en los tumores. La única vacuna de tratamiento aprobada, para el cáncer de próstata avanzado, prolonga la vida sólo 4 meses.

Algunos científicos pensaron que las vacunas contra el cáncer podrían funcionar mejor para prevenir que para tratar la enfermedad. Uno de sus defensores fue la inmunóloga oncológica de la Universidad de Pittsburgh Olivera Finn, cuyo equipo descubrió en 1989 el primer antígeno asociado a tumores: una versión de MUC1, una proteína de la superficie celular cargada de azúcar. La versión alterada señala muchos tipos de células cancerosas.


quotation mark
We’re inspired because the impact will be massive.
  • Robert Vonderheide
  • Penn Medicine

Finn developed a vaccine consisting of short stretches of MUC1. In the first study of a preventive vaccine in healthy people, she tested safety in 39 people who had previously had precancerous colon polyps, which put them at elevated risk for colon cancer. In 2013, her team reported 17 had a strong immune response, with much higher levels of antibodies to the tumor version of MUC1 than previously seen in cancer patients who got the vaccine as treatment. The other 22 people, who didn’t make antibodies, had immune-suppressing cells in their blood, apparently lingering from their removed polyps, Finn says.

The trial’s modest success led to a larger, placebo-controlled trial to see whether the vaccine prevented new polyps in people who had had them removed. This time, just 11 of 53 participants who received the vaccine produced plentiful antibodies, possibly because the patients’ immune-suppressing polyps had been removed only recently. But among the 11 responders, only three had polyps recur within 1 year of receiving the vaccine, compared with 31 of 47 participants in a placebo group, Finn’s team reports in a paper submitted to a journal.

“It was very encouraging,” Finn says. “When you have no recurrence in responders, you know the vaccine is working.” Adding a treatment that blocks immune-suppressing cells may boost response rates, she says. Her team now plans MUC1 vaccine trials for several precancerous conditions.

One drawback of Finn’s vaccine strategy is that the short proteins, or peptides, it contains mainly trigger one arm of the immune system: the B cells that make antibodies. “For immunity against cancer we really need to mobilize T cells,” says cancer immunologist Robert Vonderheide, director of Penn Medicine’s Abramson Cancer Center. That’s best done by injecting the genetic instructions for the antigen rather than the antigen itself. Special immune cells then take up the DNA or RNA, manufacture the antigen, chop it up, and display bits tailored to that person’s immune system on their cell surfaces. These antigen-presenting cells then teach T cells to recognize and kill tumor cells.

Vonderheide’s team is testing a DNA-based vaccine targeting a different antigen that marks many tumors: hTERT, a small chunk of telomerase, an enzyme that protects chromosomes as cancer cells proliferate.

Results of a trial testing the vaccine’s safety in 93 patients in remission after treatment for various cancers were encouraging. All but four people made T cells that home in on hTERT, the team reported in the Journal for ImmunoTherapy of Cancer in July 2021. And there was a hint the vaccine was warding off cancer. Among the 34 people who had had pancreatic cancer, 41% were still cancer free after 18 months. In other pancreatic cancer patients in remission, their tumor reappears within an average of 12 months.

The Penn team is now studying safety and immune responses to the vaccine in 16 people in remission from previous cancers who have inherited mutations in BRCA1 or BRCA2, relatively common cancer genes that raise risk for breast and some other cancers. Next year, the researchers expect to give the vaccine to 28 people with BRCA mutations who have never had cancer.

Cancer prevention vaccines on trial

Planned and in-progress clinical tests of vaccines to prevent cancer include the following:

 
 
Target cancers Participants Number of participants Start date Antigens Vaccine type
Breast, ovarian, prostate People with BRCA1 or BRCA2 mutations who have never had cancer or are in remission 44 April 2021 hTERT, PMSA, WNT1 DNA
Triple negative breast People in remission after treatment for triple negative breast cancer 24 October 2021 Alpha-lactalbumin Protein
Pancreatic People with an inherited mutation or family history that puts them at high risk for pancreatic cancer 25 May 2022 KRAS Peptide
Colon, endometrial, others People with Lynch syndrome who have never had cancer or are in remission 45 June 2022 Suite of 209 frameshift neoantigens Viral vector

But because hTERT is found on some normal cells as well as cancerous ones, a vaccine could trigger an autoimmune attack on healthy cells, suggests immunologist Vincent Tuohy of the Cleveland Clinic. He has devised a breast cancer prevention vaccine that may be safer because it contains a breast cell protein called alpha-lactalbumin that people only make during late pregnancy and breastfeeding. Production of the protein also occurs in triple negative breast cancer, an aggressive form of the disease. Tuohy’s team is testing whether his protein vaccine can stimulate an immune response in 24 women who have been treated for triple negative breast cancer and have no plans to get pregnant. The next step, he says, will be a trial in healthy women with BRCA1 mutations, who are prone to this cancer type.

Other teams hope to offer broader protection against breast cancer. Undeterred by being called “misguided” in 2012, NBCC is close to testing a breast cancer vaccine, initially in healthy breast cancer survivors. The advocacy group’s president, Fran Visco, says it set the ambitious goal because it was “frustrated with the lack of innovation in breast cancer.” With scientist partners, it has settled on a vaccine that combines six tumor antigens, including hTERT and MUC1. “We don’t know what type of breast cancer a woman is going to get,” explains trial leader Keith Knutson, an immunologist at the Mayo Clinic. Multipronged vaccines “are probably going to be more effective than vaccines targeting one individual protein,” says cancer immunologist Nora Disis of the University of Washington, Seattle, who is developing such a vaccine to prevent colon cancer.

As some teams are trying to broaden the immune response triggered by cancer vaccines, others want to make it safer and more precise by targeting neoantigens, only found on cancer cells. Those efforts have accelerated over the past decade thanks to a surge in tumor genome sequencing, which has revealed a flood of neoantigens. Some drive cancer growth, whereas others have no apparent function. Most are unique to an individual cancer—an obstacle for developing preventive vaccines, which have to target markers that can be predicted in advance.

Some neoantigens reliably appear on many people’s tumors, however. For instance, pancreatic cancer is almost always triggered by mutations in a growth protein called KRAS, which give rise to a predictable set of neoantigens. This spring, Johns Hopkins University immunologist Elizabeth Jaffee and colleague Neeha Zaidi will begin to safety test a vaccine containing mutated KRAS peptides in 25 men and women who haven’t had cancer but are at high risk because of an inherited mutation or family history. KRAS is like pancreatic cancer’s Achilles’ heel, Jaffee says: It’s the first of several genes to get mutated. As a result, the team hopes early tumor cells won’t be able to evade the vaccine by ditching KRAS and finding another way to grow.

Lynch syndrome cancers also sport a predictable set of neoantigens. That’s because patients’ DNA repair problem leads to “frameshift” mutations, which shift how a cell’s proteinmaking machinery reads a gene, scrambling the resulting protein in a consistent way. A peptide vaccine containing a few of these neoantigens, which was developed by a German team, caused no serious side effects when tested in people with cancer. A similar vaccine designed for mice with Lynch syndrome reduced tumor growth, researchers reported in July 2021 in Gastroenterology.

The vaccine Vilar-Sanchez’s team will test is more ambitious: It consists of viruses modified to carry DNA for a whopping 209 frameshift neoantigens found in Lynch tumors. People’s immune systems vary in how they respond to specific neoantigens, and different individuals’ tumors won’t all make the same set. “Therefore, the best [approach] is to have many,” says Elisa Scarselli, chief scientific officer of Nouscom, an Italian company developing the vaccine.

The vaccine is also being developed as treatment, and in an early test Nouscom is giving it along with an immunotherapy drug to patients who have metastatic cancers with frameshift mutations like those in Lynch syndrome. At a meeting in fall 2021, the company reported the treatment shrank tumors in seven of the first 12 patients. “We really believe we will see even more immunogenicity in healthy carriers of Lynch disease” because they should have stronger immune systems, Scarselli says.


Eduardo Vilar-Sanchez is testing a vaccine to prevent Lynch syndrome cancers.MD Anderson Cancer Center

Vilar-Sanchez’s trial, beginning within a few months, will give the vaccine to 45 volunteers with Lynch syndrome—both people in remission after cancer treatment and others who have never had tumors. Investigators will assess whether the vaccine stimulates an immune response and has any apparent effect on polyps or tumor formation.

Los esfuerzos por aprovechar el sistema inmunitario para combatir el cáncer tienen una larga historia. En la década de 1890, el médico William Coley informó de que las inyecciones de toxinas bacterianas -una especie de vacuna- a veces reducían los tumores de los pacientes, aparentemente estimulando el sistema inmunitario. Décadas más tarde, los investigadores descubrieron que las células inmunitarias llamadas células T podían reconocer los antígenos tumorales como extraños y atacar los cánceres. Este hallazgo dio lugar a dos clases de terapias aprobadas: fármacos que levantan los frenos moleculares de las células T para que puedan intensificar su ataque contra el cáncer, y células T diseñadas para atacar a las células cancerosas. Ambos tipos de tratamiento han tenido un éxito sorprendente contra ciertos tipos de cáncer.

Un tercer tipo de inmunoterapia, las vacunas para tratar el cáncer, se ha quedado atrás. Los esfuerzos despegaron a principios de la década de 1990, cuando los investigadores empezaron a contabilizar docenas de antígenos tumorales que podrían despertar las defensas inmunitarias de un paciente. A menudo estos antígenos son proteínas que las células cancerosas utilizan para crecer o propagarse, por lo que los antígenos son buenos marcadores de las células cancerosas.

Pero, a pesar de los datos prometedores de los experimentos con animales, la mayoría de las vacunas terapéuticas no han conseguido detener el crecimiento del tumor en las personas. Como los antígenos asociados a los tumores también pueden estar presentes en cantidades escasas en las células normales, el sistema inmunitario tiende a ignorarlos. La quimioterapia u otros tratamientos agresivos que reciben los pacientes con cáncer también debilitan su respuesta inmunitaria, y los tumores están protegidos por su "microambiente", es decir, células y moléculas circundantes que suprimen las células T asesinas y les impiden entrar en los tumores. La única vacuna de tratamiento aprobada, para Si los resultados parecen buenos, el siguiente paso será un estudio aleatorio de cientos de pacientes a lo largo de quizás 5 a 10 años. "Hay mucho que ganar" si la vacuna funciona, dice Vilar-Sánchez. "Una vacuna contra el cáncer no va a reducir el riesgo a cero, pero podría influir en la frecuencia con la que realizamos el cribado". También podría ayudar a las pacientes a decidir si se someten a una histerectomía para prevenir los cánceres de endometrio, que son frecuentes en las personas con síndrome de Lynch.

Todas las vacunas de prevención se enfrentarían a un largo camino hacia la aprobación reglamentaria si los investigadores deben esperar a que aparezcan tumores para juzgar la eficacia de la vacuna. Por ello, también buscarán medidas sustitutivas de protección, como la reducción del crecimiento de pólipos en personas propensas al cáncer de colon. En el caso del cáncer de mama, los investigadores aún no disponen de biomarcadores, pero esperan encontrarlos, quizá un cambio en las células inmunitarias de la sangre o en el tejido mamario, afirma Vonderheide.

"Tenemos que ser lo suficientemente inteligentes como para presentar a la FDA [Administración de Alimentos y Medicamentos de EE.UU.] un biomarcador de éxito", afirma Vonderheide. "Esto es formidable. Pero estamos inspirados porque el impacto será masivo".

Cualesquiera que sean los antígenos que prefieran, muchos científicos esperan modelar sus próximas vacunas preventivas a partir de las principales vacunas COVID-19, que utilizan una partícula lipídica para transportar el ARNm de los antígenos al interior de las células. Las vacunas de ARNm son más fáciles de fabricar y administrar que las vacunas de ADN o víricas, y la pandemia ha demostrado que en general son seguras y estimulan una fuerte respuesta. "El hecho de que las vacunas de ARNm hayan demostrado su seguridad en miles de millones de personas sanas de todas las edades hace que [el ARNm] sea una plataforma muy buena" para las vacunas preventivas contra el cáncer, afirma Jaffee.

La Casa Blanca también apuesta por las vacunas de ARNm para prevenir el cáncer. Están en la lista de posibles proyectos de un reavivado Cancer Moonshot y de la nueva agencia de investigación de alto riesgo y alta recompensa, la Agencia de Proyectos de Investigación Avanzada para la Salud (ARPA-H). Un documento conceptual para la ARPA-H expone el objetivo de la siguiente manera: "Utilizar vacunas de ARNm para enseñar al sistema inmunitario a reconocer 50 mutaciones genéticas comunes que provocan cánceres, de modo que el cuerpo elimine las células cancerosas cuando surjan por primera vez".

Esa descripción levanta algunas cejas. "Eso sería heroico", dice Finn, porque los antígenos de la vacuna tendrían que cubrir no sólo un enorme número de mutaciones del cáncer, sino también "la increíble diversidad genética" de las respuestas inmunitarias de los individuos. "No es imposible, pero no es sencillo", afirma.

El genetista clínico Steven Lipkin, de Weill Cornell Medicine, que trabaja en las vacunas contra el síndrome de Lynch, se muestra cautelosamente optimista y señala que una vacuna que redujera las tasas de los cánceres más comunes "digamos en un tercio o en la mitad en un gran número de personas sería un beneficio tremendo."

Un equipo ya está probando una vacuna para la prevención de múltiples cánceres, pero no en personas, sino en perros. En un ensayo de cinco años, un equipo está administrando a 400 perros de mediana edad una vacuna que contiene 31 antígenos de ocho cánceres caninos comunes. (Otros 400 perros reciben una vacuna placebo.) Se basa en los neoantígenos del ARN, moléculas poco estudiadas que son el resultado de errores de procesamiento del ARN y no de mutaciones del ADN. Son mucho más abundantes que los neoantígenos de ADN en los perros y las personas, y son "altamente inmunogénicos", afirma el desarrollador y bioquímico Stephen Johnston, del Instituto de Biodiseño de la Universidad Estatal de Arizona, en Tempe. Si resultan eficaces, podrían facilitar la consecución del objetivo de la Casa Blanca de desarrollar una vacuna humana contra el cáncer, afirma.


 

 

 

sábado, 26 de marzo de 2022

El conocimiento de la naturaleza de la ciencia aumenta la aceptación pública de la misma, independientemente de los factores de identidad

 

 El conocimiento de la naturaleza de la ciencia aumenta la aceptación pública de la misma, independientemente de los factores de identidad


No le digas a la gente que "confíe en la ciencia": eso los hace caer en la pseudociencia

En su lugar, enseñe cómo funciona la ciencia. A medida que las personas aprenden eso (como cómo se construyen y prueban las teorías), aceptan hallazgos válidos como el cambio climático, la evolución y las vacunas, ¡independientemente de sus puntos de vista ideológicos!

Knowledge about the nature of science increases public acceptance of science regardless of identity factors

First Published December 18, 2020 Research Article Find in PubMed

 

Aunque las opiniones de la gente sobre la ciencia están relacionadas con factores de identidad (por ejemplo, la orientación política) y con el conocimiento de las teorías científicas, el conocimiento sobre el funcionamiento de la ciencia en general también desempeña un papel importante. Para probar esta afirmación, administramos dos evaluaciones detalladas sobre las prácticas de la ciencia a una muestra demográficamente representativa del público estadounidense (N = 1500), junto con preguntas sobre la aceptación de la evolución, el cambio climático y las vacunas. Las opiniones políticas y religiosas de los participantes predijeron su aceptación de las afirmaciones científicas, como en trabajos anteriores. Pero un mayor conocimiento de la naturaleza de la ciencia y una visión más madura de cómo mitigar los desacuerdos científicos se relacionaron positivamente con la aceptación. Es importante destacar que el efecto positivo del pensamiento científico sobre la aceptación se mantuvo independientemente de la ideología política o la religiosidad de los participantes. Por tanto, una mayor atención al desarrollo del conocimiento del funcionamiento de la ciencia podría ayudar a combatir la resistencia a las afirmaciones científicas en todo el espectro político y religioso.


Traducción realizada con la versión gratuita del traductor www.DeepL.com/Translator

Some scientific claims are controversial among members of the public, especially in the United States. For example, despite overwhelming scientific consensus that evolutionary theory provides the best explanation for the origin and development of species, at least a quarter of the US public rejects this explanation (Smith and Son, 2013; Weisberg et al., 2018). In addition, there is a 37-point gap between members of the US public and members of the scientific community in terms of their acceptance of anthropogenic climate change (Pew Research Center, 2015). The same pattern can be seen with respect to vaccine safety (Pew Research Center, 2015; Villa, 2019).

Public resistance to well-established scientific claims is troubling not simply from an epistemic point of view; vaccine non-compliance, for example, has resulted in many deaths, and failure to acknowledge climate change can lead to similarly dire results. The recent (lack of) response to COVID-19 from members of the public and political leaders also underscores the ways in which science denial can have deadly consequences. It is thus imperative to identify the reasons behind people’s resistance to science and to uncover effective ways to combat it.

People’s opposition to science is often associated with identity factors, like political affiliation or religious identity (McPhetres and Zuckerman, 2018; Rutjens et al., 2018). For example, individuals who are more politically conservative and more religious tend to reject evolution at higher rates than average (Swift, 2017; Weisberg et al., 2018). Similarly, political conservatives are more likely to deny climate change (Brenan and Saad, 2018). Vaccine safety denial is similarly tied to identity factors, though these deniers hold extreme views at both ends of the political (Baumgaertner et al., 2018; Berezow and Campbell, 2012) and religious (Kennedy, 2017) spectrums.

These links between identity factors and science acceptance may occur because people’s responses to survey questions about scientific issues are subject to pressure from their group affiliations (e.g. Douglas and Wildavsky, 1982; Kahan et al., 2011; Lewandowsky et al., 2013). For example, individuals who are more religious know that religion is seen as conflicting with evolution. So they may report that they do not accept evolution when asked, regardless of their personal views, because this response conforms to the views of their religious community. If people are sensitive only to the norms of their community when deciding what they should believe, then their knowledge about science plays little role, if any. In support of this argument, some previous work has found that knowledge of evolutionary theory does not relate to acceptance of it (e.g. Bishop and Anderson, 1990; Lawson and Worsnop, 1992; Shtulman, 2006). Simply teaching people the science behind evolutionary theory, anthropogenic climate change, or vaccine safety, then, will not increase acceptance.

But there is a reason to question this skeptical conclusion. Prior work has found positive correlations between individuals’ knowledge of particular scientific theories and their acceptance of these theories (McPhetres et al., 2019; Weisberg et al., 2018). Furthermore, some studies have demonstrated that teaching the mechanisms of climate change (Ranney and Clark, 2016) and evolution (Ingram and Nelson, 2006; Lawson and Weser, 1990; Shtulman and Calabi, 2013) can increase acceptance of these theories. So, people’s knowledge about particular scientific theories, not just their identities, can matter to science acceptance.

However, much of this work has examined only how people’s knowledge about a scientific theory affects their acceptance of that particular theory. An educational strategy based on these results would thus involve teaching each theory separately. While it would be beneficial for members of the public to gain this knowledge, this strategy might not be the most efficient way to combat resistance to science. After all, it is impossible to know what sort of science knowledge may be relevant in the future, as science denial related to the current pandemic has demonstrated.

A more promising approach may thus be to focus on people’s knowledge of general science facts and of the processes and practices of science, known as the Nature of Science (NoS). In general, people who have higher NoS knowledge may be in a better position to understand the connection between scientific practices and the generation of knowledge (Nelson et al., 2019; Thanukos and Scotchmoor, 2012) or the role that the scientific community plays (Slater et al., 2019). This knowledge may allow for more robust acceptance of the scientific consensus or greater trust in scientific claims.

Indeed, several prior studies have found such a connection: People who perform better on tests of general science knowledge and reasoning are overall more likely to accept scientific claims, such as those about climate change and evolution (Lombrozo et al., 2008; McPhetres and Zuckerman, 2018; Rutjens et al., 2018; Weisberg et al., 2018). This connection presents a potentially fruitful avenue for intervention: Imparting a broad scientific knowledge base could potentially lead to greater acceptance of a variety of scientific claims without needing to address each of those claims directly. Furthermore, teaching about science in general may not encounter the kind of reflexive resistance that teaching directly about a specific controversial claim would.

But this connection between NoS knowledge and acceptance of scientific claims is more complex than it first appears. For example, the Ordinary Science Intelligence Scale (OSI) (Kahan, 2017) is a commonly used measure of NoS. It includes a subsample of basic science knowledge questions (e.g. electrons are smaller than atoms) drawn from the National Science Foundation (NSF) Science and Engineering Indicators (National Science Board, 2016). The OSI additionally includes measures of numeracy (e.g. how to express numerically a 1% chance of winning a prize if 1000 people enter a lottery), and measures of cognitive reflection (Frederick, 2005). While those who score highly on the OSI tend to accept climate change, in line with the work reviewed above, those who are additionally politically conservative are less likely to accept it (Kahan, 2015; Kahan et al., 2012). That is, greater knowledge about aspects of science actually corresponds to greater polarization in people’s views (see also Drummond and Fischhoff, 2017; Hamilton, 2011).

Why might this be the case? While greater NoS knowledge may simply lead to greater polarization overall, it is important to note that some extant measures of NoS only ask people about scientific facts, hence may not capture the most probative aspects of NoS. For example, prior work has sometimes used questions about people’s knowledge of scientific facts from the General Social Survey (e.g. True or false: More than half of human genes are identical to those of mice). While people should know these important science facts, they are simply facts, which one could memorize without really understanding. This could explain why greater knowledge of such facts does not always lead to better acceptance of scientific claims.

Other measures, including the OSI, do present questions that gauge people’s knowledge of the methods of science (e.g. the need for a control group) or people’s general thinking skills (e.g. general numeracy). But these measures do not tend to capture people’s knowledge of how science generates knowledge or how scientists carry out their work. We hypothesize that those aspects of NoS are particularly important predictors of acceptance of scientific claims, since knowledge about the way in which science works may be necessary to making productive connections between scientific claims and the process of generating and validating those claims. Conversely, individuals who have poor knowledge about how science works (e.g. that there is only a single scientific method that must be followed rigidly, like a recipe) may thereby fail to know that scientific theories are reliable, valid, and supported by multiple converging lines of evidence. This hypothesis about the connection between knowledge about the processes and practices of science and acceptance of scientific claims has so far not been fully tested on a demographically representative sample in the United States. This study aims to fill this gap. Specifically, we test whether greater knowledge about the aspects of the nature of science (NoS) described earlier could benefit people’s acceptance of several publicly controversial scientific claims (evolution, anthropogenic climate change, and vaccine safety), regardless of their political or religious views.

Furthermore, and crucially, none of this prior work has directly examined how people think about scientific disagreements and their style of resolving such disagreements. Given that public discourse about scientific topics is often framed as debates between opposing sides, gaining an understanding of how members of public conceptualize these debates is vital. Specifically, individuals who see the debates as being completely black and white—one side must be incorrect if the other side is correct—may fail to accept scientific claims that seem controversial because they lack knowledge about how such claims can be both well-supported and defeasible, or about how different interpretations of evidence could possibly be valid.

This study addresses these issues by using two new measures of people’s knowledge about these aspects of the NoS. One presents a series of 20 statements (e.g. “The process of science is nonlinear; each step can lead to many possible next steps.”) for which participants rate their agreement. These statements all focus on some aspect of how science is practiced or how theories are developed, rather than on knowledge of particular scientific facts or general thinking abilities.

Our second measure gauges participants’ epistemological styles. We present a brief vignette about a scientific disagreement, in which two groups of scientists investigated developmental deformities in a population of frogs (adapted from Barzilai and Weinstock, 2015). Some scientists had evidence that these deformities were caused by cysts in the leg area, while other scientists had evidence that these deformities were caused by chemicals in the water. Crucially, we do not ask our participants to judge which group was correct. Instead, we ask what it would take to decide which group was correct.

We do so by presenting four questions about this disagreement (e.g. “Can one know for certain what happened to the frogs?”). For each question, participants are asked to rate their level of agreement with three possible answers: “Yes. If the topic were to be investigated further, one could know for certain,” “No. Even if the topic were investigated further, one could never know for certain because it is not possible to observe what really happened,” and “Maybe. If the topic were to be investigated further, one could not be completely certain, but one could make a reasonable estimate.” Participants rate their degree of agreement with each of these answers independently, allowing us to determine how much each participant’s views align with each type of claim.

These three answers are designed to capture different epistemic styles (Kuhn et al., 2000, 2008). The first is absolutism, the idea that knowledge is objectively true and can be straightforwardly obtained from observation of the world. The second is multiplism (or relativism), the idea that knowledge is subjective because it is generated by human minds, hence any scientific view is just as valid as any other. The third is evaluativism, the idea that any body of scientific knowledge has degrees of certainty, hence scientific claims must undergo a continual process of evaluation in light of other knowledge and theories. Prior work has found this third idea is the most mature and is related to better performance on reasoning tasks for both adults and children (Kuhn et al., 2008; Thomm et al., 2017; Walker et al., 2012).

To our knowledge, these are the most nuanced measures of scientific thinking that have been presented to a representative sample of the US public, allowing us to fully explore the possibility that a general knowledge of how science works might provide an avenue toward reducing public rejection of well-supported scientific claims. It is important to note that, in contrast to prior work in this area, these two new measures do not test individuals’ knowledge of any particular scientific theory or claim, or of any discrete facts. Rather, these measures examine higher order knowledge about how science works and how scientists should resolve disputes. As such, this study provides a first window into how knowledge of the processes and practices of science could mitigate identity-based resistance to specific scientific claims, regardless of one’s knowledge about the science underlying the claims themselves.

Based on prior work, we predict that more politically conservative participants and more religious participants will tend to reject publicly controversial scientific claims. We additionally predict that both of our new measures of the NoS will be related to acceptance of scientific theories. Specifically, participants who have a better knowledge of the nature of theories and participants who have a more evaluativist style will be more likely to accept these theories. Finally, and most importantly, we predict that the relationships between politics and acceptance and between religion and acceptance will be moderated by participants’ NoS knowledge and by their epistemological styles. Participants’ knowledge about how science is practiced should provide protection against the effects of their ideology, making them less polarized in their views about scientific claims.

 

We pre-registered our hypotheses with respect to evolutionary theory (https://osf.io/y6amz); parenthetical numbering throughout the article refers to the measures, hypotheses, and analyses registered in that document. We consider our investigations with respect to climate change and vaccines exploratory.1

Participants

We contracted with YouGov, a survey firm, to recruit a sample of 1500 participants. This sample size represents the maximum number of participants YouGov could provide to us based on our available funding. The final sample included 811 women (54%) and 689 men (46%). Participants’ average age was 50 years (SD = 16.4 years, range = 18–92 years).

YouGov originally administered our survey to 1611 participants drawn from their standing panels. Then, blind to our hypotheses, they selected our 1500 final participants by matching cases to a sampling frame on the variables of gender, age, race, education, political party identification, political ideology, and political interest. This sampling frame was constructed from the 2010 American Community Survey, the November 2010 Current Population Survey, and the 2007 Pew Religious Life Survey.

Measures

Participants completed 13 measures (pre-registration section 11). In this article, we focus on the following five: evolution acceptance (11.11), climate change acceptance (11.5), vaccine acceptance (11.7), knowledge of the NoS (11.1), and epistemic thinking style (11.2). The remaining eight measures asked about participants’ views on the consequences of accepting the theory of evolution, the conflict between science and religion, the appropriate expert (scientific, religious, or other) to consult about a set of questions, the reasons that they might accept a claim, the reasons that they might consider a particular claim to be true, whether they identify as a particular kind of person (e.g. a science person, an arts person), and knowledge of evolutionary theory. See the Supplemental materials or the pre-registration site (https://osf.io/y6amz) for the exact text of all questions. As some of these measures were drawn from prior work, we followed those studies’ practices with respect to randomization or counterbalancing of questions and answer options within each block.

Evolution acceptance

This multiple-choice question asked participants to choose which of the following options best describes how they think animals and plants (n = 740) or human beings (n = 760) came to exist on earth: (a) they were created by God in more or less their current form (creationist), (b) they developed through natural processes, which were guided by God the entire time (theist), (c) they developed through natural processes, which were set up by God but continued on their own (deist), or (d) they developed entirely through natural processes (naturalist). These answer options appeared in this order for all participants, following previous surveys of evolution acceptance that also presented the choices as decreasing in their level of supernatural involvement (e.g. the Gallup poll). Although three of these four answer options explicitly reference God, we based the wording of this question on previous measures of public acceptance of evolution and on our own piloting, both of which found that a majority of participants assent to God having some involvement in the process of evolution.

Climate change acceptance

We presented three questions about climate change (based on wording used by the Pew Research Center). All participants first responded to the question, “From what you’ve read and heard, is there solid evidence that the average temperature on earth has been getting warmer over the past few decades?” This question had three answer choices: “Yes, there is solid evidence that the earth is getting warmer”; “No, there is no solid evidence that the earth is getting warmer”; and “Don’t know.”

Participants who responded “yes” to this first question were then asked to choose the primary cause of climate change from the following options: “Human activity such as burning fossil fuels”; “Natural patterns in the earth’s environment”; and “Don’t know.” Participants who responded “no” to the first question were asked to choose whether we just do not know enough yet about whether the earth is getting warmer or whether the earth just is not getting warmer, or they could indicate that they did not know. For all three questions, the first two options were presented in a random order.

Vaccine acceptance

We presented participants with a single question asking whether childhood vaccines were safe. There were four answer options: “very safe,” “somewhat safe,” “not very safe,” and “not safe at all.” As with the evolution acceptance question, these options were always presented in the same order, since they have a natural logical progression.

Nature of science index

We presented participants with 20 statements about the practice of science and the nature of scientific theories (Hofer, 2000; Liang et al., 2006; Lombrozo et al., 2008; Schommer, 1990).2 For example, “The same hypothesis or theory is often tested in many different ways” and “Scientific theories are just scientists’ guesses” (reverse-scored). For each statement, participants rated their level of agreement on a five-point scale: strongly disagree, disagree, unsure, agree, and strongly agree. The order of the 20 statements was randomized between participants.

Epistemic thinking style

This measure (based on Barzilai and Weinstock, 2015) first presented participants with a description of two theories about the causes of deformities in a population of frogs. This description was followed by four general questions about the nature of knowledge and how knowledge should be justified (e.g. “Must there be only one true explanation about the deformed frogs?”). These four questions were presented in a random order for each participant.

Each of these four questions had three possible answers, and these answers each reflected one of the three epistemological styles: absolutism, multiplism, and evaluativism. Participants used a scale from 1 (“very much disagree”) to 10 (“very much agree”) to rate their agreement with each statement. As in Barzilai and Weinstock (2015), these three statements were presented in a random order for each participant, and each statement was presented on a separate page in order to encourage participants to respond independently to each.

Procedure

Participants completed the survey online. Each of the 12 measures appeared as its own block in the survey. These blocks were presented in a random order except for the block about evolution acceptance, which always appeared last. This was done so as not to bias responses to our set of questions about evolution knowledge, which was a focus of our pre-registered analyses.

Questions about demographic factors (e.g. age, gender, political orientation) were presented on their own in a separate testing session before participants engaged in this survey. Responses from that session were used to construct a demographically representative sample, as noted earlier.

Coding and descriptive statistics

Evolution acceptance

We first tested whether there were differences in responses to the “humans” and “plants and animals” versions of this question. We found overall differences in the distribution of responses among our four acceptance categories (χ2(3) = 20.09, p < .001). Specifically, the “humans” wording of the question received significantly more creationist responses than the “plants and animals” version (36.6% vs 26.4%; exact proportions test p < .001), significantly fewer deistic responses (17.4% vs 22.6%; exact proportions test p < .001), and marginally fewer naturalistic responses (30.9% vs 35.7%; exact proportions test p = .057). This aligns with other work showing that different versions of an acceptance question can yield different responses, particularly when comparing humans to other living things (Maitland et al., 2014; Miller et al., 2006). Given that participants responded generally similarly to the two versions of the question, and for ease of interpretation, we combined their responses into a single acceptance measure for our main analyses.

We found that 31.5% of participants agreed with the creationist option, 15.3% of participants agreed with the theist option, 20.0% of participants agreed with the deist option, and 33.3% of participants agreed with the naturalistic option.

For our main regression analyses, we split the four response options to this question into two categories: “created by God” and “guided by God” were coded as “leans creationist” (0) and “set up by God” and “natural processes” were coded as “leans evolutionist” (1). We pre-registered the analysis using this coding strategy because these pairs of categories tended to cohere and because the binary outcome variable is easier to interpret than the relational outcomes. Overall, 53.3% of our participants were categorized as leaning evolutionist.

Climate change acceptance

We used responses to the three climate change questions to construct a scale of responses (1–7), with higher numbers indicating closer agreement to the scientific consensus of anthropogenic climate change. Participants who responded “yes” to the first question (i.e. there is solid evidence that the Earth is getting warmer) and then attributed that fact to human activity were assigned the highest score (7) since this matches the scientific consensus. Participants who responded “yes” to the first question and then attributed that fact to natural patterns were assigned a score of 6. Participants who responded “yes” to the first question but then said they did not know why this was happened were assigned a score of 5. Participants who responded “don’t know” to the first question were coded as 4. Participants who responded “no” to the first question (i.e. there is no solid evidence that the Earth is getting warmer) but then said they did not know why were assigned a score of 3. Participants who responded “no” to the first question and then said that we just do not know enough yet were assigned a score of 2. Participants who responded “no” to the first question and then said that the Earth just is not getting warmer were assigned a score of 1.

The average overall score on this scale was 5.1 (SD = 2.1), significantly higher than the midpoint of the scale (4; t(1499) = 20.6, p < .001). We found that 62.5% of our population said that they accepted climate change, indicating that a majority of US citizens agree with the scientific consensus on this issue. These numbers are generally in line with reports from other polls: Gallup, for example finds that 66% of the population accepts that climate change is happening (Brenan and Saad, 2018; see also Leiserowitz et al., 2010). In addition, 45.9% of our population agreed that climate change is caused by human activity.

As with evolution acceptance, we created a binary acceptance variable to use in our main analyses. Participants who responded “yes” to the first question (i.e. there is solid evidence that the Earth is getting warmer, in agreement with the scientific consensus) were assigned a score of 1. All other participants were assigned a score of 0.

Vaccine acceptance

We coded participants’ responses so that higher scores were assigned to answers that more closely reflected the scientific consensus (as we did with climate change). Responses of “not safe at all” were coded 1, “not very safe” were coded 2, “somewhat safe” were coded 3, and “very safe” were coded 4. One participant who skipped this question was removed from analyses that used this scale.

Overall, 88.9% of our participants accepted the safety of vaccines, with 53.1% of all participants saying that vaccines were very safe. These numbers align well with a 2016 Pew poll, in which 88% of US respondents judged vaccines to be safe (Villa, 2019). The average score on our acceptance scale for vaccines was 3.38 (SD = 0.79), which is significantly higher than the midpoint of the scale (2.5; t(1498) = 42.99, p < .001).

We again created a binary variable for analysis, with scores of 1 and 2 reflecting overall non-acceptance (coded 0) and scores of 3 and 4 reflecting overall acceptance (coded 1).

Nature of science index

We converted participants’ responses to the 20 items into a scale from 1 (strongly disagree) to 5 (strongly agree). Eight of the items were reverse coded. Each participant’s responses to these 20 items were averaged into a single score, with higher numbers reflecting a greater knowledge about NoS. We examined the unity of this index using the nFactors package in R. An analysis of eigenvalues, a parallel analysis, and an optimal coordinates analysis suggested a three-factor solution (see Table 1), whereas the acceleration factor suggested a one factor solution. Next, we conducted an exploratory factor analysis specifying three factors using the psych package in R. Examining the factor loadings (see Table 1) suggests that the factors correspond to (1) a recognition that science is an ongoing and potentially nonlinear process (11 items), (2) (not) viewing science as a set, stable method (seven items), and (3) (not) dismissing science as mere guesswork (two items).

Table

Table 1. Factor loadings for the Nature of Science index. Loadings below 0.30 are not displayed.

Table 1. Factor loadings for the Nature of Science index. Loadings below 0.30 are not displayed.

It is worth noting that although three factors were suggested, the factors appeared to break down based on whether the items were reverse coded. Given this and the fact that internal consistency for the entire index was strong (Cronbach’s alpha = .84), we chose to retain all items in for analyses. Average score on this index was 3.73 (SD = 0.45). Although this is significantly above the midpoint of the index (2.5; t(1499) = 106.66, p < .001), the distribution of responses is roughly normal.

Epistemic thinking style

This measure asked participants their level of agreement with 12 statements, four for each of the three epistemic thinking styles (absolutist, multiplist, and evaluativist). Each participant’s responses to the four statements reflecting each style was averaged together, creating three scores per participant. Following the study on which this measure was based (Barzilai and Weinstock, 2015), these averages ranged from 1 to 10, with higher numbers reflecting a greater degree of agreement with each thinking style. One participant failed to respond to one of the evaluativism items, so this missing value was filled in with the mean of the sample for that question before constructing this participant’s evaluativism summary score.

Overall scores on the absolutism scale (M = 6.55, SD = 1.47) and on the evaluativism scale (M = 7.01, SD = 1.45) were significantly above the midpoint of the scale (5.5; t(1499) = 27.55, p < .001 and t(1499) = 40.17, p < .001, respectively). Scores on the multiplism scale (M = 4.81, SD = 1.80) were significantly below the midpoint (t(1499) = −14.78, p < .001). Cronbach’s alpha for the absolutism scale was .52, for the multiplism scale was .66, and for the evaluativism scale was .62. Although these alpha values are somewhat low, we chose to use these scales as they were presented in order to remain consistent with prior work using this measure.

Political orientation

Participants were asked to rate their ideology on a five-point scale, which we scored from 1 (“very liberal”) to 5 (“very conservative”). There were 162 participants who responded “not sure”; their data were removed from analyses involving this scale. We found that 13.1% of our participants reported being very liberal, 16.7% liberal, 33.2% moderate, 23.5% conservative, and 13.5% very conservative. The average overall score on this scale was 3.08 (SD = 1.21), significantly higher (i.e. more conservative) than the midpoint of the scale (t(1337) = 2.29, p = .02).

For data visualization (although not for analyses), we transformed this into a three-point scale by labeling participants who responded “very liberal” or “liberal” as liberal and participants who responded “conservative” or “very conservative” as conservative.

Religiosity

Participants responded to three questions from the Pew Religious Life battery, which asked about their frequency of attendance at religious services, the importance of religion in their lives, and their frequency of prayer. Responses to these three items were made on different scales. To combine them into a single scale, we first normalized the scale for each item. Then we averaged these scores together and normalized this composite scale, which we used in our analyses. Because we normalized the scale, the average was 0 and SD was 1.

For data visualization only, we split this scale into three groups, with participants responding more than one SD above M being labeled “highly religious” (25% of the sample), participants responding between one SD above and below M being labeled “average religious” (50% of the sample), and participants responding more than one SD below M being labeled “low religious” (25% of the sample).

Table 2 provides a correlation matrix for all variables.

Table

Table 2. Zero-order correlations among all variables.

Table 2. Zero-order correlations among all variables.

Acceptance of evolutionary theory (pre-registered analyses)

Individual predictors

We examined the likelihood that participants leaned evolutionist conditional on their political ideology, religiosity, knowledge of the NoS, and their epistemic thinking styles (absolutism, multiplism, and evaluativism scores). Separate logistic regression analyses were conducted to characterize the relationship between each variable and evolution acceptance (see sections 4.1.6, 4.2, and 17.2 in our pre-registration).

As predicted, conservative political ideology (b = −0.66, p < .001; hypothesis 4.2.2.3) and greater religiosity (b = −1.39, p < .001; hypothesis 4.2.2.2) were associated with a decreasing likelihood of leaning evolutionist. Greater NoS knowledge was associated with an increasing likelihood of leaning evolutionist (b = 1.61, p < .001; hypothesis 4.2.1.4). Increasing evaluativism predicted a greater likelihood of leaning evolutionist (b = 0.14, p < .001; hypothesis 4.2.1.8), whereas increasing multiplism predicted a lower likelihood of leaning evolutionist (b = −0.33, p < .001; hypothesis 4.2.1.7). Contrary to our predictions, absolutism was unrelated to whether participants leaned evolutionist (b = −0.01, p = .774; hypothesis 4.2.1.7).

Conditional effects

We next examined whether the relations between leaning evolutionist and NoS knowledge, and between leaning evolutionist and having an evaluativist thinking style, were conditional on the identity variables (political orientation and religiosity) (hypothesis 4.1.7). We conducted logistic regression analyses predicting the degree of leaning evolutionist from our two measures of science epistemology and from the two identity variables, including the interaction terms. Here, following our pre-registration (section 17.1), we examined relations with political ideology and religiosity separately.

In terms of political ideology, the probability of leaning evolutionist increased with increasing NoS knowledge (odds ratio 38.7) and with increasing evaluativist thinking (odds ratio 1.07) for each level of political orientation (Figure 1, top panels). In addition, we found that the relationship between leaning evolutionist and NoS knowledge was conditional on political ideology (b = −0.67, p < .001), such that greater political conservatism was associated with a weaker influence of NoS knowledge on leaning evolutionist. However, the relationship between leaning evolutionist and evaluativism was not conditional on political ideology (b = 0.003, p = .929): Increasing one’s commitment to an evaluativist thinking style increased the likelihood of leaning evolutionist equally across the political spectrum.


                        figure

Figure 1. Relations between evolution acceptance, science epistemology measures, and demographic factors. Shaded areas represent 95% confidence intervals.

As with political ideology, the probability of leaning evolutionist increased with increasing NoS knowledge (odds ratio 4.42) and with increasing evaluativist thinking (odds ratio 1.18) for each level of religiosity (Figure 1, bottom panels). The relationship between leaning evolutionist and NoS knowledge was conditional on religiosity (b = −0.50, p = .005); the predicted probability of leaning evolutionist increased with increasing NoS knowledge of the NoS even for those who scored in the top 25% of our measure of religiosity, but their increase was less steep. The relationship between leaning evolutionist and evaluativism was also conditional on religiosity (b = −0.12, p = .013) with the probability of leaning evolutionist increasing with greater evaluativist thinking only for those with middle to lower religiosity scores.

Acceptance of climate change (exploratory analyses)

Individual predictors

In parallel to our analyses of evolution acceptance, we conducted separate logistic regression analyses predicting our binary climate change acceptance variable from the other variables individually. Because these analyses were not pre-registered, we used a Bonferroni correction to adjust our alpha level to .0083, which accounts for the six tests that we ran. We found that conservative political ideology (b = −1.05, p < .001) and greater religiosity (b = −0.50, p < .001) were significantly associated with a decreasing likelihood of accepting climate change. Greater knowledge of the NoS (b = 1.82, p < .001), increasing absolutism (b = 0.21, p < .001), and increasing evaluativism (b = 0.31, p < .001) predicted a greater likelihood of acceptance. Increasing multiplism predicted a lower likelihood of acceptance (b = −0.18, p < .001).

Conditional effects

As for evolution acceptance, increasing NoS knowledge (odds ratio 48.8) and increasing agreement with evaluativist statements (odds ratio 1.52) was associated with an increased likelihood of accepting climate change across all levels of political orientation. This pattern also held across all levels of religiosity (odds ratio 5.66 for NoS knowledge and 1.38 for evaluativism) (Figure 2). Again, we used a Bonferroni correction to adjust the alpha level to account for multiple comparisons across these four tests (new alpha = .0125).


                        figure

Figure 2. Relations between climate change acceptance, science epistemology measures, and demographic factors. Shaded areas represent 95% confidence intervals.

We additionally found that the relationship between NoS knowledge and accepting climate change was conditional on political ideology (b = −0.74, p < .001), whereas the relationship between evaluativist thinking and accepting human-caused climate change was not (b = −0.05, p = .26). Likelihood of acceptance increased with increasing NoS knowledge and increasing evaluativist thinking style for each of the political leanings. This increase was sharper for liberals than for conservatives, but only for the NoS index.

The relationship between accepting climate change and NoS knowledge was also conditional on religiosity (b = −0.64, p < .001), but the relationship between accepting climate change and evaluativism was not (b = −0.06, p = .12). The predicted probability of accepting climate change increased with increasing NoS knowledge and with increasing evaluativist thinking, even for those who scored in the top 25% of our measure of religiosity. This increase was sharper for low-religiosity individuals than for high-religiosity individuals, but only for the NoS index.

Acceptance of the safety of vaccines (exploratory analyses)

Individual predictors

With an adjusted alpha level of .0083, conservative political ideology (b = −0.33, p < .001) was significantly associated with a decreasing likelihood of accepting that vaccines are safe. Greater NoS knowledge (b = 1.50, p < .001) and increased evaluativism significantly predicted acceptance of vaccines’ safety (b = 0.32, p < .001). Greater religiosity (b = −0.08, p = .34), absolutism (b = 0.07, p = .19), and multiplism (b = −0.06, p = .21) were not significant predictors.

Conditional effects

As in our climate change analyses, we adjusted our alpha level of .0125 to account for multiple comparisons. Both increasing NoS knowledge and increasing evaluativism were associated with increased probability of acceptance across the political and religious spectrum (Figure 3). The likelihood of accepting that vaccines are safe increased with increasing NoS knowledge (odds ratio 8.3), and this relationship did not differ across all levels of political ideology (b = −0.19, p = .34). The same was true for the relationship between vaccine acceptance and evaluativism (odds ratio 1.86), which also did not significantly differ based on political ideology (b = −0.12, p = .035).


                        figure

Figure 3. Relations between vaccine acceptance, science epistemology measures, and demographic factors. Shaded areas represent 95% confidence intervals.

In terms of religiosity, the relationship between vaccine acceptance and NoS knowledge was significantly conditional on religiosity (b = −0.56, p = .007). Although individuals at all levels of religiosity increased their likelihood of accepting vaccines’ safety with increasing NoS knowledge (odds ratio 4.3), individuals of high religiosity experienced the increase in acceptance with increasing NoS knowledge at a less dramatic rate (see Figure 3, bottom panels). The relationship between vaccine acceptance and an evaluativist thinking style was not significantly conditional on religiosity (b = −0.07, p = .18); individuals across the religious spectrum were more likely to accept vaccines’ safety with increasing evaluativism (odds ratio 1.39).

 

 


Funding
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the National Science Foundation (SES-1455425).

ORCID iDs
Deena Skolnick Weisberg https://orcid.org/0000-0002-4000-4941

Asheley R. Landrum https://orcid.org/0000-0002-3074-804X

Jesse Hamilton https://orcid.org/0000-0002-6571-4325

Michael Weisberg https://orcid.org/0000-0002-3944-1167

Supplemental material
Supplemental material for this article is available online.


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Author biographies

Deena Skolnick Weisberg is an Assistant Professor in the Department of Psychological and Brain Sciences at Villanova University, where she directs the Scientific Thinking and Representation (STAR) Laboratory and co-directs the Pennsylvania Laboratory for Understanding Science (PLUS). Her research focuses on scientific thinking and imaginative cognition in children and adults. She has published over 50 peer-reviewed articles and her work has received funding from the National Science Foundation and the Templeton Foundation.

Asheley R. Landrum is an assistant professor of science communication in the College of Media and Communication at Texas Tech University. Prior to this, she was a Howard Deshong Postdoctoral Fellow at the Annenberg Public Policy Center of the University of Pennsylvania. Her research focuses on the role of individuals’ views and values in their interpretation of scientific information and she is currently a principal investigator on two National Science Foundation grants examining young adults’ engagement with educational science media.

Jesse Hamilton is a doctoral student in Philosophy at the University of Pennsylvania. Jesse focuses on ethics, political philosophy, and philosophy of science. His specific research interests within those areas include human rights, distributive justice, just war, and climate change.

Michael Weisberg is a Professor and Chair of Philosophy, as well as Senior Faculty Fellow and Director of Post-Graduate Programs at Perry World House, at the University of Pennsylvania. His research focuses on how highly idealized models and simulations can be used to understand complex systems. He leads efforts to better understand the interface between humans and wildlife and between humans and the climate system, and he studies how scientific issues are understood by communities in the Americas and in East Asia.