Abstract
Latent varicella zoster virus (VZV) has been detected in human adrenal glands, raising the possibility of virus-induced adrenal damage and dysfunction during primary infection or reactivation. Rare cases of bilateral adrenal hemorrhage and insufficiency associated with VZV reactivation have been reported. Since there is no animal model for VZV infection of adrenal glands, we obtained adrenal glands from two non-human primates (NHPs) that spontaneously developed varicella from primary simian varicella virus (SVV) infection, the NHP VZV homolog. Histological and immunohistochemical analysis revealed SVV antigen and DNA in the adrenal medulla and cortex of both animals. Adrenal glands were observed to have Cowdry A inclusion bodies, cellular necrosis, multiple areas of hemorrhage, and varying amounts of polymorphonuclear cells. No specific association of SVV antigen with βIII-tubulin-positive nerve fibers was found. Overall, we found that SVV can productively infect NHP adrenal glands, and is associated with inflammation, hemorrhage, and cell death. These findings suggest that further studies are warranted to examine the contribution of VZV infection to human adrenal disease. This study also suggests that VZV infection may present itself as acute adrenal dysfunction with “long-hauler” symptoms of fatigue, weakness, myalgias/arthralgias, and hypotension.
Highlights
We examined the immunohistopathological characteristics of adrenal glands if simian varicella virus (SVV) is associated with nerve fibers, adrenal glands were immunostained for the presence containing SVV antigen in two macaques with varicella
Caque, SVV antigen was detected within the cortex and medulla, along with necrosis detected predominantly in the cortex and hemorrhage throughout
SVV antigen was present in the cortex and corticomedullary junctions but absent in the medulla; more hemorrhage and necrosis were seen throughout
Summary
Varicella zoster virus (VZV; human herpesvirus 3) is an exclusively human, doublestranded DNA virus that infects >90% of the world population. Primary infection occurs after exposure to aerosolized virus or vesicular fluid from individuals with varicella (chicken pox) or herpes zoster (shingles). VZV replicates in the upper respiratory mucosal epithelial cells, spreads to tonsils and other lymphoid tissue, and infects T cells. Infected T cells enter the bloodstream and transport VZV to the skin, causing a widespread rash (varicella) (reviewed in [1]). The virus enters sensory neurons of the cranial, dorsal root, autonomic, and enteric ganglia to establish latency through infected T cells or by retrograde transport of virions from infected skin [2,3,4,5,6].
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