Aruna Subramanian y Taia T. Wang. DOI:https://doi.org/10.1016/j.chom.2021.06.018
Recopilado por Carlos Cabrera Lozada. Director del postgrado de Medicina Materno Fetal. Universidad Central de Venezuela. ORCID: 0000-0002-3133-5183. 20/07/2021
Summary
Severe COVID-19 arises from the convergence of inadequate pre-existing immunity and a host response that damages, rather than repairs, tissues. We outline clinical presentations of COVID-19 that are likely driven by dysregulated host immunity, discuss potential mechanisms underlying pathological responses, and highlight important areas for basic research on this topic.
The substantial mortality in coronavirus disease 2019 (COVID-19) has been driven largely by an absence of pre-existing immunity that could have provided some protection in vulnerable populations against severe and fatal outcomes. As population immunity increases in some regions, severe COVID-19 has become much less frequent; yet communities lacking protection continue to be ravaged by this disease. In addition to vaccines, having medications that prevent the acute respiratory distress syndrome (ARDS) that is often central in fatal COVID-19 could dramatically reduce the threat of SARS-CoV-2 as a human pathogen. For this reason, understanding mechanisms involved in the pathogenesis of severe COVID-19 is imperative.