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Sci Signal ; 16(782): eabq1366, 2023 04 25.
Artigo em Inglês | MEDLINE | ID: mdl-37098119

RESUMO

Macrophages are key cellular contributors to the pathogenesis of COVID-19, the disease caused by the virus SARS-CoV-2. The SARS-CoV-2 entry receptor ACE2 is present only on a subset of macrophages at sites of SARS-CoV-2 infection in humans. Here, we investigated whether SARS-CoV-2 can enter macrophages, replicate, and release new viral progeny; whether macrophages need to sense a replicating virus to drive cytokine release; and, if so, whether ACE2 is involved in these mechanisms. We found that SARS-CoV-2 could enter, but did not replicate within, ACE2-deficient human primary macrophages and did not induce proinflammatory cytokine expression. By contrast, ACE2 overexpression in human THP-1-derived macrophages permitted SARS-CoV-2 entry, processing and replication, and virion release. ACE2-overexpressing THP-1 macrophages sensed active viral replication and triggered proinflammatory, antiviral programs mediated by the kinase TBK-1 that limited prolonged viral replication and release. These findings help elucidate the role of ACE2 and its absence in macrophage responses to SARS-CoV-2 infection.


Assuntos
COVID-19 , SARS-CoV-2 , Humanos , SARS-CoV-2/fisiologia , Enzima de Conversão de Angiotensina 2/genética , Citocinas , Peptidil Dipeptidase A/genética , Peptidil Dipeptidase A/metabolismo , Macrófagos/metabolismo , Vírion/metabolismo
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