Varicella zoster virus reactivation following COVID-19 vaccination: a report of 3 cases.

BACKGROUND: The advent of vaccination against COVID-19 brought great expectations for the control of the pandemic. As novel vaccines, much of the associated side effects were unknown. Currently, an increasing number of reports from side effects of COVID-19 vaccines have been published, namely on cutaneous reactions. These are of utmost importance to increase our knowledge about possible undesirable effects and its prevention. METHODS: We describe a series of 3 cases who presented with varicella zoster virus (VZV) reactivation following the first dose of 3 different COVID-19 vaccines. RESULTS: Three patients sought their Family Doctor after developing typical lesions of VZV reactivation, following a period of 3-13 days after COVID-19 vaccination. None was under immunosuppressive therapy. The 3 patients recovered in a few weeks and the subsequent doses of the vaccines were administered, without recurrence of the symptoms. CONCLUSIONS: These cases highlight the possibility of VZV reactivation after the first dose of COVID-19 vaccines. Family Doctors should be aware of this event and play an important role informing and reassuring local communities for this possible vaccine reaction.

Mycobacterium tuberculosis Strains Are Differentially Recognized by TLRs with an Impact on the Immune Response.

Tuberculosis associates with a wide spectrum of disease outcomes. The Beijing (Bj) lineage of Mycobacterium tuberculosis (Mtb) is suggested to be more virulent than other Mtb lineages and prone to elicit non-protective immune responses. However, highly heterogeneous immune responses were reported upon infection of innate immune cells with Bj strains or stimulation with their glycolipids. Using both in vitro and in vivo mouse models of infection, we here report that the molecular mechanism for this heterogeneity may be related to distinct TLR activations. Among this Mtb lineage, we found strains that preferentially activate TLR2, and others that also activate TLR4. Recognition of Mtb strains by TLR4 resulted in a distinct cytokine profile in vitro and in vivo, with specific production of type I IFN. We also uncover a novel protective role for TLR4 activation in vivo. Thus, our findings contribute to the knowledge of the molecular basis underlying how host innate immune cells handle different Mtb strains, in particular the intricate host-pathogen interaction with strains of the Mtb Bj lineage.