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

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.

Risk Factors of Severe COVID-19: A Review of Host, Viral and Environmental Factors

“…Interactions Between Risk Factors of Severe COVID-19 ). Furthermore, SARS-CoV-2 infection has been reportedly connected to the reactivation of latent hepatitis virus [ 546 ] and Mycobacterium tuberculosis infections [ 442 , 547 ].…”

Cardiovascular and haematological pathology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): A role for viruses

“…Incidentally, SARS-CoV-2 infection leads to the reactivation of herpesviruses, specifically EBV [ [247] , [248] , [249] ]. Reactivation of these viruses and the subsequent maladaptation of physiological systems, including the immune, endocrine, and nervous system, are believed to be important steps in ME/CFS pathology [ 3 , 60 , 250 ].…”

SARS‐CoV‐2 is capable of reactivating orocutaneous opportunistic infections in vaccinated patient: A case report

“…The association between SARS-CoV-2 and herpesviruses has been observed in several patients, although the pathophysiological mechanisms involved in the process of herpes zoster (HZ) lytic reactivation remain poorly understood. 3,4 It is estimated that approximately 60% of severe cases of SARS-CoV-2-positive patients may show risk of coinfection. 4 Some authors debate that neurotropism of novel coronavirus by peripheral nervous system may be attributed to linkage Neuropilins 1 and 2 (NRP1 and NRP2).…”

“…3,4 It is estimated that approximately 60% of severe cases of SARS-CoV-2-positive patients may show risk of coinfection. 4 Some authors debate that neurotropism of novel coronavirus by peripheral nervous system may be attributed to linkage Neuropilins 1 and 2 (NRP1 and NRP2). These receptors act as an additional gateway for the virus and, consequently, interact with nociceptors and disturb nervous tissue electrophysiology.…”