The COVID-19 infection produces an immunosuppressive state due to functional impairment and a concomitant quantitative decrease in T lymphocytes, particularly CD4+ T cells, CD8+ T cells, and natural killer cells which could be the plausible mechanism for the increased susceptibility to herpes zoster reactivation in COVID-19 patients [12]. Few studies have reported the reactivation of numerous other viruses, including human herpesvirus 6, 7, and Epstein-Barr virus, after COVID-19 infection [13]. This evidence concerns the gene CD8A and COVID-19.