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Determinantes genéticos e inmunológicos humanos de la neumonía crítica por COVID-19

Qian Zhang^1,2,3, Paul Bastard^4,5,6,7,

¹St Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA. qzhang02@rockefeller.edu.

|January 28, 2022

Resumen

Los factores genéticos y autoinmunes que afectan a los interferones de tipo I (IFN) explican al menos el 15% de los casos críticos de neumonía por COVID-19. La inmunidad insuficiente de IFN tipo I en el tracto respiratorio puede conducir a enfermedades graves, influenciadas por la edad y el sexo.

Área de la Ciencia:

Inmunología
Virología
La genética

Sus antecedentes:

La infección por SARS-CoV-2 generalmente es leve, pero el 10% desarrolla neumonía hipoxémica, y el 3% está gravemente enfermo.
El riesgo de mortalidad aumenta con la edad y es mayor en los varones.

Objetivo del estudio:

Revisar los factores moleculares y celulares que determinan la neumonía crítica por el COVID-19.
Para identificar las causas genéticas y autoinmunes del SARS-CoV-2 grave.
Comprender el papel de los interferones tipo I (IFN) en la patogénesis del COVID-19.

Principales métodos:

Revisión de la literatura existente sobre los determinantes moleculares y celulares de la neumonía crítica por COVID-19.
Análisis de la prevalencia de errores congénitos y autoanticuerpos contra los IFN de tipo I en pacientes críticos con COVID-19.

Principales resultados:

Se encontraron errores congénitos de IFN tipo I (deficiencias de TLR3, TLR7) en el 1-5% de los pacientes con neumonía crítica menores de 60 años.
Los autoanticuerpos que neutralizan los IFN de tipo I (IFNα, IFNβ, IFNω) se encuentran en el 15-20% de los pacientes con neumonía crítica mayores de 70 años.
Al menos el 15% de los casos críticos de neumonía por COVID-19 se explican por estos defectos inmunológicos relacionados con el IFN.

Conclusiones:

La inmunidad IFN tipo I, particularmente la producción dependiente de TLR3/TLR7, es crucial para la defensa del huésped contra el SARS-CoV-2.
La inmunidad insuficiente del IFN tipo I al comienzo de la infección puede conducir a la propagación viral y a una inflamación grave.
La edad y el sexo influyen en la prevalencia y el impacto de estos defectos inmunológicos en el COVID-19 crítico.

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