COVID-19 y Errores innatos de la inmunidad, enfermedades autoinmunes e inmunosupresión
Resumen
La pandemia de COVID-19 llegó a cinco olas en tres años con más de 6.5 millones de muertes en todo el mundo. Conocer la susceptibilidad diferencial al nuevo betacoronavirus ha permitido comprender mejor la fisiopatología y sus complicaciones inflamatorias, así como disecar la respuesta inmunitaria. En este proceso, destaca el papel de linfocitos T CD8+ y NK, así como sensores virales, interferones tipo 1, inflamación exagerada a cargo de NLRP3 y tormenta de citocinas IL-6 e IL-18. La secuenciación de todo el exoma ha permitido identificar varios genes con variantes germinales patogénicas en pacientes con COVID-19 grave; dichos genes explicarían alrededor del 5% de los casos graves. Además, hasta el 20% de adultos hospitalizados albergan autoanticuerpos contra interferones. Estos hallazgos traducen nuevas etiologías genéticas y los autoanticuerpos explican el peor pronóstico en ancianos, asociado al fenómeno inflammaging. En general, a los pacientes con inmunodeficiencias que adquirieron la COVID-19 no les fue peor, con una supervivencia global mayor al 80% y un predominio de cuadros leves. La excepción fueron pacientes con inmunodeficiencia combinada grave o con síndrome poliglandular autoinmune 1, estos últimos porque desarrollan autoanticuerpos contra interferón. En pacientes con enfermedades autoinmunes o trastornos autoinflamatorios tampoco se ha reportado mayor gravedad. Sin embargo, aquéllos que reciben inmunosupresores suelen tener un cuadro prolongado. Los pacientes con ganancia de función de NLRP3 y STAT1 pueden ser especialmente susceptibles a complicaciones inflamatorias sistémicas. En esta revisión documental resumimos la experiencia global en la atención de pacientes con alteraciones inmunitarias que se infectaron por SARS-CoV-2.Citas
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