RESUMO
Resumen La infección por SARS-CoV-2 promueve un descontrol del sistema inmune con predominio de una respuesta inflamatoria de rápida instauración y el desencadenamiento de una tormenta de citocinas. El objetivo de esta revisión es comprender mejor los mecanismos inmunológicos y su descontrol activados por SARS-CoV-2. La activación de la inmunidad innata, contra la infección, es el factor clave para el control viral o su progresión hacia COVID-19. La respuesta inmune adaptativa, igualmente es perturbada por SARS-CoV-2 con lo cual se posibilita una mayor tasa de infección, así como también el descontrol inmunológico sistémico que puede desencadenar shock y daño tisular en diferentes órganos, muerte por COVID-19 o autoinmunidad post COVID-19.
Abstract The SARS-CoV-2 infection promotes a lack of control of the immune system with a predominance of a rapidly onset inflammatory response and the triggering of a cytokine storm. The objective of this review is to understand better the immune mechanisms and their lack of control activated by SARS-CoV-2. The activation of innate immunity against infection is the key factor for viral control or its progression towards COVID-19. The adaptive immune response is also disturbed by SARS-CoV-2, which enables a higher infection rate, as well as systemic immune lack of control that can trigger shock and tissue damage in different organs, death from COVID-19 or autoimmunity post-COVID-19.
RESUMO
BACKGROUND: Chagas disease is caused by Trypanosoma cruzi, and humans acquire the parasite by exposure to contaminated feces from hematophagous insect vectors known as triatomines. Triatoma virus (TrV) is the sole viral pathogen of triatomines, and is transmitted among insects through the fecal-oral route and, as it happens with T. cruzi, the infected insects release the virus when defecating during or after blood uptake. METHODS: In this work, we analysed the occurrence of anti-TrV antibodies in human sera from Chagas disease endemic and non-endemic countries, and developed a mathematical model to estimate the transmission probability of TrV from insects to man, which ranged between 0.00053 and 0.0015. RESULTS: Our results confirm that people with Chagas disease living in Bolivia, Argentina and Mexico have been exposed to TrV, and that TrV is unable to replicate in human hosts. CONCLUSIONS: We presented the first experimental evidence of antibodies against TrV structural proteins in human sera.