Molecular Biology Of Varicella Zoster Virus Infection

National Institute Of Allergy And Infectious Diseases

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Abstract

Varicella-zoster virus (VZV) establishes latency in human sensory and cranial nerve ganglia during primary infection (varicella), and the virus can reactivate and cause zoster after primary infection. Unlike infections in humans where large quantities of cell-free virus are released, infection in vitro does not result in release of cell-free virus. Thus, better models are needed that recapitulate observations of VZV in humans. Autophagy is a cellular process in which cellular components are degraded and recycled. VZV has been shown to induce autophagy in transformed cells and keratinocytes. We observed autophagy in skin organ cultures between 14 and 28 days after infection with VZV; in contrast, autophagy in uninfected skin organ cultures was minimal. The results in VZV-infected skin organ cultures were similar to those observed in biopsies from persons with herpes zoster. Autophagy was induced at a similar level in cells infected with wild-type VZV or in cells infected with recombinant VZV expressing the herpes simplex virus (HSV) ICP34.5 gene which inhibits autophagy in cells infected with HSV. Thus, the autophagy blocking function of the HSV ICP34.5 gene was not active during VZV infection.