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Review
. 2022 Nov;94(11):5103-5111.
doi: 10.1002/jmv.27994. Epub 2022 Jul 22.

SARS-CoV-2 infection and lytic reactivation of herpesviruses: A potential threat in the postpandemic era?

Affiliations
Review

SARS-CoV-2 infection and lytic reactivation of herpesviruses: A potential threat in the postpandemic era?

Jungang Chen et al. J Med Virol. 2022 Nov.

Abstract

The outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the causative pathogen for the coronavirus disease 2019 (COVID-19) pandemic, has greatly stressed our healthcare system. In addition to severe respiratory and systematic symptoms, several comorbidities increase the risk of fatal disease outcomes, including chronic viral infections. Increasing cases of lytic reactivation of human herpesviruses in COVID-19 patients and vaccinated people have been reported recently. SARS-CoV2 coinfection, COVID-19 treatments, and vaccination may aggravate those herpesvirus-associated diseases by reactivating the viruses in latently infected host cells. In this review, we summarize recent clinical findings and limited mechanistic studies regarding the relationship between SARS-CoV-2 and different human herpesviruses that suggest an ongoing potential threat to human health in the postpandemic era.

Keywords: COVID-19; SARS-CoV-2; herpesvirus; lytic; pandemic.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of potential mechanisms for Kaposi's sarcoma‐associated herpesvirus (KSHV) reactivation by SARS‐CoV‐2 coinfection or anti‐COVID‐19 drugs. The arrows and bars represent the activation and inhibition, respectively. Notably, the mechanisms of KSHV regulation of angiotensin‐converting enzyme 2 expression remain unknown. N, nucleocapsid protein; S, spike protein.
Figure 2
Figure 2
Schematic diagram of potential mechanisms for Epstein–Barr virus (EBV) reactivation by SARS‐CoV‐2 coinfection or anti‐COVID‐19 drugs. The arrows and bars represent the activation and inhibition, respectively. The mechanisms of Molnupiravir downregulating EBV lytic genes remain unclear.

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