RESUMEN
The coronavirus disease (Covid-19) pandemic is the most serious event of the year 2020, causing considerable global morbidity and mortality. The goal of this review is to provide a comprehensive summary of reported associations between inter-individual immunogenic variants and disease susceptibility or symptoms caused by the coronavirus strains severe acute respiratory syndrome-associated coronavirus, severe acute respiratory syndrome-associated coronavirus-2, and two of the main respiratory viruses, respiratory syncytial virus and influenza virus. The results suggest that the genetic background of the host could affect the levels of proinflammatory and anti-inflammatory cytokines and might modulate the progression of Covid-19 in affected patients. Notably, genetic variations in innate immune components such as toll-like receptors and mannose-binding lectin 2 play critical roles in the ability of the immune system to recognize coronavirus and initiate an early immune response to clear the virus and prevent the development of severe symptoms. This review provides promising clues related to the potential benefits of using immunotherapy and immune modulation for respiratory infectious disease treatment in a personalized manner.
Asunto(s)
COVID-19/inmunología , Síndrome de Liberación de Citoquinas/inmunología , Predisposición Genética a la Enfermedad , Gripe Humana/inmunología , Infecciones por Virus Sincitial Respiratorio/inmunología , Síndrome Respiratorio Agudo Grave/inmunología , Antivirales/uso terapéutico , Variación Biológica Individual , COVID-19/genética , COVID-19/virología , Síndrome de Liberación de Citoquinas/tratamiento farmacológico , Síndrome de Liberación de Citoquinas/genética , Síndrome de Liberación de Citoquinas/virología , Expresión Génica , Humanos , Inmunidad Innata , Factores Inmunológicos/uso terapéutico , Gripe Humana/tratamiento farmacológico , Gripe Humana/genética , Gripe Humana/virología , Lectina de Unión a Manosa/genética , Lectina de Unión a Manosa/inmunología , Orthomyxoviridae/efectos de los fármacos , Orthomyxoviridae/inmunología , Infecciones por Virus Sincitial Respiratorio/tratamiento farmacológico , Infecciones por Virus Sincitial Respiratorio/genética , Infecciones por Virus Sincitial Respiratorio/virología , Virus Sincitiales Respiratorios/efectos de los fármacos , Virus Sincitiales Respiratorios/inmunología , Coronavirus Relacionado al Síndrome Respiratorio Agudo Severo/efectos de los fármacos , Coronavirus Relacionado al Síndrome Respiratorio Agudo Severo/inmunología , SARS-CoV-2/clasificación , SARS-CoV-2/efectos de los fármacos , SARS-CoV-2/inmunología , Síndrome Respiratorio Agudo Grave/tratamiento farmacológico , Síndrome Respiratorio Agudo Grave/genética , Síndrome Respiratorio Agudo Grave/virología , Receptores Toll-Like/genética , Receptores Toll-Like/inmunología , Tratamiento Farmacológico de COVID-19RESUMEN
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes novel coronavirus disease (COVID-19), is the seventh pathogenic coronavirus recently discovered in December 2019 in Wuhan, China. To date, our knowledge about its effect on the human host remains limited. It is well known that host genetic factors account for the individual differences in the susceptibility to infectious diseases. The genetic susceptibility factors to COVID-19 and its severity are associated with several unanswered questions. However, the experience gained from an earlier strain of coronavirus, SARS-CoV-1, which shows 78% genetic similarity to SARS-CoV-2 and uses the same receptor to bind to host cells, could provide some clues. It, therefore, seems possible to assemble new evidence in order to solve a potential genetic predisposition puzzle for COVID-19. In this chapter, the puzzle pieces, including virus entry receptors, immune response, and inflammation-related genes, as well as the probable genetic predisposition models to COVID-19, are discussed.