tetano
Editor, Senior Moderator
J Med Microbiol
. 2025 Jun;74(6).
doi: 10.1099/jmm.0.002016. SARS-CoV-2 and neurotropism: evidence, gaps and reflections
Thaísa Regina Rocha Lopes[SUP] 1 2 [/SUP], Bibiana Santana Sitton[SUP] 3 4 [/SUP], Micheli Mainardi Pillat[SUP] 3 4 5 [/SUP], Carlos Fernando Mello[SUP] 3 4 [/SUP], Rudi Weiblen[SUP] 1 [/SUP], Eduardo Furtado Flores[SUP] 1 [/SUP], José Valter Joaquim Silva Júnior[SUP] 1 3 4 5 6 [/SUP]
Affiliations
Coronavirus disease 2019 (COVID-19) patients may present with a wide clinical spectrum, including extrapulmonary involvement, such as neurological damage. Although the pathogenesis of neurological COVID-19 still remains unclear, some studies have discussed the potential association between tissue injury and severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) infection in the central nervous system (CNS) and/or immune imbalance. These two mechanisms are non-mutually exclusive; however, exacerbated inflammatory-response-induced neurological damage appears to be more aligned with COVID-19 pathogenesis, whereas SARS-CoV-2 infection/replication in the CNS remains widely discussed. Herein, we dissect this last issue, highlighting some evidence on SARS-CoV-2 neuroinvasion, as well as discussing gaps that should be addressed for a better understanding of its potential neurotropism, specifically in the CNS. Finally, we propose some deeper reflections on the SARS-CoV-2 neurotropic potential.
Keywords: coronavirus; coronavirus disease 2019 (COVID-19); tropism.
. 2025 Jun;74(6).
doi: 10.1099/jmm.0.002016. SARS-CoV-2 and neurotropism: evidence, gaps and reflections
Thaísa Regina Rocha Lopes[SUP] 1 2 [/SUP], Bibiana Santana Sitton[SUP] 3 4 [/SUP], Micheli Mainardi Pillat[SUP] 3 4 5 [/SUP], Carlos Fernando Mello[SUP] 3 4 [/SUP], Rudi Weiblen[SUP] 1 [/SUP], Eduardo Furtado Flores[SUP] 1 [/SUP], José Valter Joaquim Silva Júnior[SUP] 1 3 4 5 6 [/SUP]
Affiliations
- PMID: 40522851
- DOI: 10.1099/jmm.0.002016
Coronavirus disease 2019 (COVID-19) patients may present with a wide clinical spectrum, including extrapulmonary involvement, such as neurological damage. Although the pathogenesis of neurological COVID-19 still remains unclear, some studies have discussed the potential association between tissue injury and severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) infection in the central nervous system (CNS) and/or immune imbalance. These two mechanisms are non-mutually exclusive; however, exacerbated inflammatory-response-induced neurological damage appears to be more aligned with COVID-19 pathogenesis, whereas SARS-CoV-2 infection/replication in the CNS remains widely discussed. Herein, we dissect this last issue, highlighting some evidence on SARS-CoV-2 neuroinvasion, as well as discussing gaps that should be addressed for a better understanding of its potential neurotropism, specifically in the CNS. Finally, we propose some deeper reflections on the SARS-CoV-2 neurotropic potential.
Keywords: coronavirus; coronavirus disease 2019 (COVID-19); tropism.