ReviewJournal of neurovirology2026
HSV-1 and VZV co-reactivation: implications for worsening neurological and neurodegenerative diseases.
Review in Journal of neurovirology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
4 authors.
Funding
Abstract
Herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) are neurotropic human alphaherpesviruses that establish lifelong latency in peripheral ganglia. While traditionally studied in isolation, increasing evidence indicates that co-reactivation of these viruses may be clinically significant, especially in the context of aging and immunosuppression, and underdiagnosed. Recent studies show that both viruses can reside in the same trigeminal ganglion (TG) and interact synergistically to potentiate and exacerbate neurological and neurodegenerative disease. This review summarizes emerging insights into the clinical, immunological, and neuropathological implications of HSV-1 and VZV co-reactivation, with a particular emphasis on VZV-derived extracellular vesicles (EVs) as mediators of immune suppression and enhancers of secondary HSV-1 infection.
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