Study finds protein behind shingles spread

Researchers at the University of Colorado Anschutz Medical Campus reported that a protein from the virus that causes shingles can hitch a ride inside tiny cell-derived particles and help the virus spread beyond the original infection site. The findings were published on July 25, 2024 in the Journal of Virology and were highlighted again by Pharmacy Times on May 22, 2026. The study focused on varicella-zoster virus, or VZV, the virus that causes chickenpox and later can reactivate as shingles. The researchers said the work identifies a previously undescribed immune-evasion mechanism used before full viral infection takes hold. ### What exactly did the researchers find inside these vesicles? The Journal of Virology study identified a viral protein called immediate-early 62, or IE62, inside small extracellular vesicles, often shortened to sEVs. Those vesicles are membrane-bound particles released by cells and can move biological cargo between cells. The researchers said IE62 was packaged into these vesicles and transported away from infected cells. (pharmacytimes.com) The University of Colorado Anschutz team used human neurons and rodent models to trace how that cargo moved. Their report said the vesicle-carried IE62 could penetrate other cells and suppress antiviral defenses, creating conditions that help VZV spread. ### Why does that matter for shingles rather than just chickenpox? Varicella-zoster virus is the same virus behind both chickenpox and shingles. (journals.asm.org) After an initial infection, the virus can remain latent in sensory neurons and later reactivate as herpes zoster, or shingles. The paper said VZV reactivation is usually seen in a unilateral dermatomal distribution, but it can also be linked to complications beyond the rash itself. (news.cuanschutz.edu) ScienceDaily, summarizing the university findings, said the newly described mechanism may help explain how the virus affects tissues far from the original site of infection. That account matched the university release, which said the vesicles may allow the virus to influence distant tissues without relying only on direct spread of infectious virus particles. ### How is this different from the usual picture of viral spread? (journals.asm.org) The study said VZV is generally understood to spread mainly through direct cell-to-cell contact. The authors wrote that immune evasion before virion entry had not been fully explained and described that gap as important to understanding VZV pathogenesis. Their findings point to non-infectious vesicles as another route by which the virus can prepare nearby or distant cells for infection. (sciencedaily.com) Pharmacy Times said the work helps explain both how the virus spreads and how antiviral responses are suppressed in infected cells. The underlying paper framed that process as an exploitation of the host cell’s small extracellular vesicle machinery. ### Who conducted the work? The paper lists Christy S. Niemeyer, Seth Frietze, Christina Coughlan, Serena W.R. (journals.asm.org) Lewis, Sara Bustos Lopez and other co-authors, with Ravi Mahalingam and Andrew N. Bubak among the named researchers. Maria A. Nagel was also listed among the authors. The study was published by the American Society for Microbiology’s Journal of Virology. The University of Colorado Anschutz release said the work was carried out by scientists at the campus and described the findings as the first identification of the mechanism allowing VZV to spread far from the infection site. (pharmacytimes.com) That characterization came from the institution’s summary of the paper. ### What comes next for readers tracking this research? (journals.asm.org) The Journal of Virology paper remains the primary source for the findings, under the title “Suppression of the host antiviral response by non-infectious varicella zoster virus extracellular vesicles.” Pharmacy Times linked to that study in its May 22, 2026 item. Any next step on treatment or prevention would depend on follow-up research testing whether blocking IE62 packaging or vesicle transport changes disease spread. That last point is an inference from the mechanism described in the paper, not a reported clinical result. (news.cuanschutz.edu) (pharmacytimes.com)