Ronaldo B. Martins

TL;DR: It is described that SARS-CoV-2 triggers the release of ACE2-depended neutrophil extracellular traps (NETs) that mediate lung pathology, supporting the use of NETs inhibitors for COVID-19 treatment.

TL;DR: This work shows that inflammasomes are activated in response to SARS-CoV-2 infection in vitro and in COVID-19 patients, contributing to the exacerbated inflammatory response, impacting disease progression and clinical outcome.

TL;DR: It is shown that astrocytes are susceptible to SARS-CoV-2 infection through a noncanonical mechanism that involves spike–NRP1 interaction and respond to the infection by remodeling energy metabolism, which in turn alters the levels of metabolites used to fuel neurons and support neurotransmitter synthesis.

TL;DR: In this study, in vitro infection of whole PBMCs from healthy donors was productive of virus progeny and results revealed that monocytes, as well as B and T lymphocytes, are susceptible to SARS-CoV-2 active infection and viral replication was indicated by detection of double-stranded RNA.

TL;DR: The data support the model where SARS-CoV-2 reaches the brain, infects astrocytes and triggers neuropathological changes that contribute to the structural and functional alterations in the brain of COVID-19 patients.