ABSTRACT
Herpes zoster (HZ) is associated with substantial morbidity. It is caused by reactivation of the latent varicella zoster virus (VZV) following decline in cell-mediated immunity, which is commonly age-related, but also occurs in individuals with immunosuppressive diseases and/or treatment. Since coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, has been associated with T cell immune dysfunction and there have been reports of HZ in COVID-19 patients, we have performed a review of available literature on whether COVID-19 could trigger HZ. We identified 27 cases of HZ following COVID-19, which most frequently occurred within 1-2 weeks of COVID-19, and the majority of cases had typical presentation. Atypical presentations of HZ were noted especially in patients with lymphopenia. It has been hypothesized that VZV reactivation occurs as a consequence of T cell dysfunction (including lymphopenia and lymphocyte exhaustion) in COVID-19 patients. Based on current evidence, which is limited to case reports and case series, it is not possible to determine whether COVID-19 increases the risk of HZ. Practitioners should be aware of the possible increased risk of HZ during the pandemic period and consider timely therapeutic and preventive measures against it.
ABSTRACT
BACKGROUND: Varicella-zoster virus (VZV) is a human neurotropic virus that remains in a latent state within ganglionic neurons throughout the entire neuroaxis after the primary infection. When herpes zoster (HZ) leads to trigeminal involvement, the ophthalmic division is the most implicated. COVID-19 has emerged as a viral cause of severe acute respiratory syndrome that has spread all over the world in the last months. Co-infection with COVID-19 and other viruses has been reported, but sparsely, and involving the respiratory viruses. METHODS: The case of a co-infection of COVID-19 with VZV is reported, and the literature reviewed. RESULTS: A 39-year-old immunocompetent man presented with oligosymptomatic infection with COVID-19, which evolved to left facial HZ, affecting the three divisions of the trigeminal nerve. The co-infection was remotely registered, being the respiratory viruses, especially influenza, the most commonly cited association. However, the present case illustrates the emergence of a latent virus infection, which might be favored by the inflammatory response to the former agent (COVID-19). This reaction ascended from the nasal cavity, where trigeminal branches are also placed. CONCLUSIONS: The emergence of latent VZV infection in this rare presentation might illustrate an effect, at least locally, of COVID-19. This virus possibly induced a retrograde reactivation of VZV in a young immunocompetent patient.