Coronavirus disease 2019 (COVID-19) is a fatal respiratory illness caused by newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The SARS-CoV-2 pandemic has caused unprecedented global health and financial burden. SARS-CoV-2 can disproportionally infect individuals leading to broad clinical outcomes ranging from moderate illness to severe pneumonia with systemic involvement. COVID-19 disease severity and mortality can be explained in part by the influence of pre-existing chronic viral infections. It is likely that SARS-CoV-2 triggers “latent” viruses, probably more in immunocompromised individuals and the recently published clinical findings show a possible link between SARS-CoV-2 infection and the reactivation of Epstein-Barr virus (EBV), cytomegalovirus (CMV), and herpes simplex virus (HSV). Potential contributors to SARS-CoV-2-linked reactivation include hypoxia, immune dysregulation, and inflammation. Interestingly, EBV, HSV, and CMV reactivation in COVID-19 patients may be associated with disease severity, poor outcome, or increased risk of hospitalization; however, a definite conclusion is yet to be drawn. Paradoxically HIV-infected individuals are not as affected by SARS-CoV-2 as had originally been anticipated. Therefore, elucidating the impact of SARS-CoV-2-triggered reactivation of latent virus on COVID-19 pathogenesis and possible involvement in long COVID will help develop newer targets for combinatorial antiviral interventions. We welcome submissions of original research, review, mini-review, perspective, and opinion articles involving basic and translational research investigations addressing the above topics. The potential articles could cover cellular, immunological, pathophysiological, and epidemiological factors that mediate SARS-CoV-2 reactivation of persistent infections in COVID-19 and long COVID manifestations.
