New insights into the pathogenesis of SARS-CoV-2 during and after the COVID- 19 pandemic
Resumen
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible
for the respiratory distress condition known as COVID-19. This disease broadly
affects several physiological systems, including the gastrointestinal, renal, and
central nervous (CNS) systems, significantly influencing the patient’s overall
quality of life. Additionally, numerous risk factors have been suggested,
including gender, body weight, age, metabolic status, renal health, preexisting
cardiomyopathies, and inflammatory conditions. Despite advances in
understanding the genome and pathophysiological ramifications of COVID-19,
its precise origins remain elusive. SARS-CoV-2 interacts with a receptor-binding
domain within angiotensin-converting enzyme 2 (ACE2). This receptor is
expressed in various organs of different species, including humans, with
different abundance. Although COVID-19 has multiorgan manifestations, the
main pathologies occur in the lung, including pulmonary fibrosis, respiratory
failure, pulmonary embolism, and secondary bacterial pneumonia. In the post-
COVID-19 period, different sequelae may occur, which may have various causes,
including the direct action of the virus, alteration of the immune response, and
metabolic alterations during infection, among others. Recognizing the serious
adverse health effects associated with COVID-19, it becomes imperative to
comprehensively elucidate and discuss the existing evidence surrounding this viral infection, including those related to the pathophysiological effects of the
disease and the subsequent consequences. This review aims to contribute to a
comprehensive understanding of the impact of COVID-19 and its long-term
effects on human health.
