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Journal Article Review Ppublish 1 citation

PubMed: 39207648 DOI: 10.1007/s11357-024-01323-9

Human herpesvirus reactivation and its potential role in the pathogenesis of post-acute sequelae of SARS-CoV-2 infection.

Geroscience 47(1):167-187

Authors: Zsófia Gáspár, Bálint Gergely Szabó, Andrea Ceglédi, Botond Lakatos

Affiliations

  • School of PhD Studies, Semmelweis University, Üllői Street 26, 1085, Budapest, Hungary.
  • South Pest Central Hospital, National Institute of Haematology and Infectious Diseases, Albert Flórián Street 5-7, 1097, Budapest, Hungary.
  • School of PhD Studies, Semmelweis University, Üllői Street 26, 1085, Budapest, Hungary.
  • South Pest Central Hospital, National Institute of Haematology and Infectious Diseases, Albert Flórián Street 5-7, 1097, Budapest, Hungary.
  • Departmental Group of Infectious Diseases, Department of Internal Medicine and Haematology, Semmelweis University, Albert Flórián Street 5-7, 1097, Budapest, Hungary.
  • Departmental Group of Infectious Diseases, Department of Internal Medicine and Haematology, Semmelweis University, Albert Flórián Street 5-7, 1097, Budapest, Hungary.

Abstract

The emergence of SARS-CoV-2 has precipitated a global pandemic with substantial long-term health implications, including the condition known as post-acute sequelae of SARS-CoV-2 infection (PASC), commonly referred to as Long COVID. PASC is marked by persistent symptoms such as fatigue, neurological issues, and autonomic dysfunction that persist for months beyond the acute phase of COVID-19. This review examines the potential role of herpesvirus reactivation, specifically Epstein-Barr virus (EBV) and cytomegalovirus (CMV), in the pathogenesis of PASC. Elevated antibody titers and specific T cell responses suggest recent herpesvirus reactivation in some PASC patients, although viremia is not consistently detected. SARS-CoV-2 exhibits endothelial trophism, directly affecting the vascular endothelium and contributing to microvascular pathologies. These pathologies are significant in PASC, where microvascular dysfunction may underlie various chronic symptoms. Similarly, herpesviruses like CMV also exhibit endothelial trophism, which may exacerbate endothelial damage when reactivated. Evidence suggests that EBV and CMV reactivation could indirectly contribute to the immune dysregulation, immunosenescence, and autoimmune responses observed in PASC. Additionally, EBV may play a role in the genesis of neurological symptoms through creating mitochondrial dysfunction, though direct confirmation remains elusive. The reviewed evidence suggests that while herpesviruses may not play a direct role in the pathogenesis of PASC, their potential indirect effects, especially in the context of endothelial involvement, warrant further investigation.

MeSH

Sars-Cov-2, Aging, Pathology, Herpesviridae, Signs And Symptoms, Aged, Herpesvirus 4, Human, Covid-19, Viruses, Severe Acute Respiratory Syndrome-Related Coronavirus, Infections, Post-Acute Covid-19 Syndrome

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