Dr. Mikolaj Raszek discussed a large study that highlighted reports of varicella-zoster virus (VZV), which causes herpes zoster (HZ, synonym: shingles), after COVID-19 inoculation.
“Shingles can be observed post-vax, COVID-19 vaccines as well, and this is actually a very well established symptom already,” Raszek said.
“In one recent publication that involved more than one million individuals, so it was a very large study. They showed that the likelihood of developing shingles post-vaccine is twice as high,” he added.
“In a vaccinated population, shingles was occurring about 0.2% of the population as opposed to 0.1% of the population that was unvaccinated,” Raszek explained.
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From the study published in the Journal of The European Academy of Dermatology and Venereology:
After matching, each cohort accounted for 1 095 086 patients. For the vaccinated group (Cohort I), 2204 subjects developed HZ within 60 days of COVID-19 vaccination, while among Cohort II, 1223 patients were diagnosed with HZ within 60 days after having visited the clinic for any other reason (i.e. not vaccination). The risk of developing shingles was calculated as 0.20% and 0.11% for cohort I and cohort II, respectively. The difference was statistically highly significant (P < 0.0001; log-rank test). The risk ratio and odds ratio were 1.802 (95% confidence interval [CI] = 1.680; 1.932) and 1.804 (95% CI = 1.682; 1.934).
Consistent with the hypothesis, a higher incidence of HZ was statistically detectable post-COVID-19 vaccine. Accordingly, the eruption of HZ may be a rare adverse drug reaction to COVID-19 vaccines. Even though the molecular basis of VZV reactivation remains murky, temporary compromising of VZV-specific T-cell-mediated immunity may play a mechanistic role in post-vaccination pathogenesis of HZ. Note that VZV reactivation is a well-established phenomenon both with infections and with other vaccines (i.e. this adverse event is not COVID-19-specific).
The present study sought to determine whether the frequency of herpes-zoster diagnoses was higher among patients who received COVID-19 vaccines (Cohort I) vs. those who were not vaccinated (Cohort II). We anticipated that the incidence of HZ might be detectably higher in Cohort I vs. Cohort II, based on prior reports by others and what is generally known about herpesviridae reactivation phenomena. The hypothesis was confirmed, based on comparative analysis of a 60-day period after vaccination (for Cohort I) vs. the same time period after a visit to the HCO for any other reason (Cohort II). Accordingly, reactivation of the varicella-zoster virus appears to be a potential ADR to COVID-19 vaccines, at least for mRNA LNP-based formulations. This finding concurs with recent reports (cited in the Introduction), a significant difference being that the present work is on a broader scale (volume of cases and distributed internationally) vs. what was sampled in other recent reports. However, we cannot draw conclusions from our analysis of the vector-based (vs mRNA-based) vaccines, as only 1.51% of the subjects in Cohort I received Ad26.COV2.S.
Intriguingly, a generally increased incidence of herpes virus infections has been reported since the COVID-19 pandemic began.42, 43 The possibility has been raised that herpesviridae reactivation may be triggered by suppressive effects of SARS-CoV-2 on a host immune system; furthermore, pandemic-related psychological stress has been noted to potentially play a causal role, too.31 On the other hand, vaccination against COVID-19 seems to potentially raise the risk of precipitating HZ. While the specific molecular mechanisms that cause VZV to reactivate remain unknown, certain risk factors have been identified—including stress, elevated age, usage of immunosuppressants, chemotherapy and radiotherapy. A unifying thread among these conditions is that they correspond to a decreased immune competence, in terms of immunoglobulins, CD4+ and CD8+ T lymphocytes and memory T cells.44 In the context of the present study, we note that innate- or cell-mediated immune failures, caused by a host’s response to COVID-19 vaccination, have been raised as potentially causative factors for VZV reactivation.38 Psichogiou et al. postulated a temporary incapacity of VZV-specific CD8+ T cells, allowing VZV to reactivate and thereby cause HZ.25
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