Human cytomegalovirus infection of epithelial cells increases SARS-CoV-2 superinfection by upregulating the ACE2 receptor.
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Perera MR, Greenwood EJ, Crozier TW, Elder EG, Schmitt J, Crump CM, Lehner PJ, Wills MR, Sinclair JH
The Journal of Infectious Diseases - (-) - [2022-11-21; online 2022-11-21]
SARS-CoV-2, the causative agent of COVID-19, has caused widespread morbidity and mortality since its onset in late 2019. Here, we demonstrate that prior infection with human cytomegalovirus (HCMV) substantially increases infection with SARS-CoV-2 in vitro. HCMV is a common herpesvirus carried by 40-100% of the population which can reactivate in the lung under inflammatory conditions, such as those resulting from SARS-CoV-2 infection. We show in both endothelial and epithelial cell types that HCMV infection upregulates ACE2, the SARS-CoV-2 cell entry receptor. These observations suggest that HCMV reactivation events in the lung of healthy HCMV carriers could exacerbate SARS-CoV-2 infection and subsequent COVID-19 symptoms. This effect could contribute to the disparity of disease severity seen in ethnic minorities and those with lower socio-economic status, due to their higher CMV seroprevalence. Our results warrant further clinical investigation as to whether HCMV infection influences the pathogenesis of SARS-CoV-2.
PubMed 36408607
DOI 10.1093/infdis/jiac452
Crossref 10.1093/infdis/jiac452
pii: 6835053