Chicken Pox - Varicella Zoster Virus
Chicken Pox - Varicella Zoster Virus
Oct 6, 2011
Introduction
Varicella zoster virus (VZV) is one of eight herpes viruses known to cause childhood chicken pox. After primary infection of the host immune system, the virus becomes latent in the dorsal root ganglia and reactivates later to cause shingles and other neurologic complications (Arvin, 1996). The virus is transmitted by airborne viral particles or through contact of vesicular fluid from an infected contact (Arvin, 1996). VZV enters the respiratory tract and infects the mucous membrane while spreading to regional lymph nodes where viral proliferation occurs in T-cells of the blood (Moffat, 2003). Primary viremia carries the virus to the liver or other cells of the mononuclear phayocyte system (Arvin,
1996). During this 2 to 3 week incubation period, a fever develops and within a few days a second round of VZV viremia infects the epidermis, producing the typical vesicular lesions of chicken pox (Hambleton, 2005). The itchy rash appears and eventually turns into fluid-filled blisters that dry and form scabs. VZV can then travel from the skin to sensory nerves, characterizing the early stage of latent neuronal infection (Hambleton, 2005).
Varicella-Zoster Virus Virology and Genome Sequence
VZV is the smallest of human alphaherpesviruses, consisting of an envelope encasing a nucelocapsid surrounding the single double stranded DNA molecule (Hambleton, 2005). VZV encodes at least 70 genes that are classified into immediate early (IE), early (E) and late (L) genes. IE and E code for nonstructural proteins that regulate viral transcription and replication. L genes code for structural proteins such as nucleocapsids, and several glycoproteins allowing VZV to spread without its viral envelope (Hambleton, 2005). These proteins code for VZV entry into host cells, bondage to a cellular receptor, and transport of the virus to the cell surface allowing it to fuse into adjacent cells
(Arvin,
Oct 6, 2011
Introduction
Varicella zoster virus (VZV) is one of eight herpes viruses known to cause childhood chicken pox. After primary infection of the host immune system, the virus becomes latent in the dorsal root ganglia and reactivates later to cause shingles and other neurologic complications (Arvin, 1996). The virus is transmitted by airborne viral particles or through contact of vesicular fluid from an infected contact (Arvin, 1996). VZV enters the respiratory tract and infects the mucous membrane while spreading to regional lymph nodes where viral proliferation occurs in T-cells of the blood (Moffat, 2003). Primary viremia carries the virus to the liver or other cells of the mononuclear phayocyte system (Arvin,
1996). During this 2 to 3 week incubation period, a fever develops and within a few days a second round of VZV viremia infects the epidermis, producing the typical vesicular lesions of chicken pox (Hambleton, 2005). The itchy rash appears and eventually turns into fluid-filled blisters that dry and form scabs. VZV can then travel from the skin to sensory nerves, characterizing the early stage of latent neuronal infection (Hambleton, 2005).
Varicella-Zoster Virus Virology and Genome Sequence
VZV is the smallest of human alphaherpesviruses, consisting of an envelope encasing a nucelocapsid surrounding the single double stranded DNA molecule (Hambleton, 2005). VZV encodes at least 70 genes that are classified into immediate early (IE), early (E) and late (L) genes. IE and E code for nonstructural proteins that regulate viral transcription and replication. L genes code for structural proteins such as nucleocapsids, and several glycoproteins allowing VZV to spread without its viral envelope (Hambleton, 2005). These proteins code for VZV entry into host cells, bondage to a cellular receptor, and transport of the virus to the cell surface allowing it to fuse into adjacent cells
(Arvin,
References: Arvin, A.M. (1996). Varicella-Zoster Virus. Clinical Microbiology Reviews, 9: 361-381. Cohen, J. I.(2010). The Varicella-Zoster Virus Genome (Berlin: Springer Berlin Heidelberg) Fine, P. E. M. (1993). Herd Immunity: History, Theory, Practice. Epidem. Hambleton S., Gershon, A. A. (2005). Preventing Varicella-Zoster Disease Moffat, J. F., Taylor, S.L., Leisenfelder, S. (2003). Viral and Cellular Kinases Play A Central Role in VZV Pathogenesis and are Targets for Antiviral Reichelt, M., Brady, J., Arvin, A. M. (2009). The Replication Cycle of Varicella-Zoster Virus: Analysis of the Kinetics of Viral Protein Expression,