Molecular Biology Of Varicella Zoster Virus Infection

National Institute Of Allergy And Infectious Diseases

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Abstract

Primary infection with varicella-zoster virus (VZV) causes chickenpox, and reactivation of the virus from latency results in zoster. Previously we identified viral genes that are required or dispensable for latency, and we have been studying the functions of the viral proteins that are important for latency. Viruses which are deleted for some of these proteins are impaired for latency and may serve as safer vaccine candidates. [unreadable] [unreadable] We have previously identified a cellular protein, insulin-degrading enzyme (IDE), that interacts with a VZV glycoprotein, gE and functions as a receptor for entry of the virus into cells. We are currently identifying how IDE performs its entry mediator activity. [unreadable] [unreadable] VZV can cause life threatening infections in immunocompromised persons. Some of these persons present with severe abdominal pain, due to reactivation of VZV in the nervous system of the intestines, and these patients may or may not develop a rash later in their course of the disease. If treatment is delayed, up to half of patients with this condition can die.[unreadable] [unreadable] We have helped to develop an assay to quantify the amount of VZV DNA in the blood of patients using quantitative PCR. Using this test we were able to detect VZV DNA in the blood of a transplant patient with abdominal pain who did not have a rash. Detection of VZV DNA led to early treatment with antiviral medication. Subsequently the patient developed a rash typical of disseminated chickenpox. Early detection of VZV allowed prompt treatment which likely resulted in a more rapid recovery. Quantification of VZV DNA in the blood can also be used to determine the optimal duration of antiviral therapy.