The pathogenesis of varicella-zoster virus neurotropism and infection
Neurotropic Viral Infections: Volume 2: Neurotropic Retroviruses, DNA Viruses, Immunity and Transmission, Page: 135-173
2016
- 3Citations
- 14Captures
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Book Chapter Description
Varicella-zoster virus (VZV) is both a neurotropic and lymphotropic human alphaherpesvirus that causes varicella, which is commonly known as chickenpox, as the primary infection in susceptible individuals. During primary infection, VZV gains access to sensory ganglia of the peripheral nervous system and establishes latency within neurons. VZV reactivation from latency causes herpes zoster, called “shingles," and is associated with a vesicular rash localized to one of the cutaneous dermatomes. While the clinical manifestations of varicella and herpes zoster are well documented, knowledge about the mechanisms of VZV pathogenesis in the human host is limited because infections are rarely fatal and VZV is highly species-specific for the human host. VZV infection of human (hu) dorsal root ganglia (DRG), skin, and thymus/liver (T cell) xenografts in the severe combined immunodeficiency (SCID) mouse model has provided a system for investigating molecular mechanisms of VZV pathogenesis. SCIDhu xenografts are infected with recombinant VZV mutant viruses that have targeted deletions or mutations of specific genes or their promoters, which enables the assessment of functions of VZV protein subdomains during VZV replication in intact human tissues in vivo. Use of these models has provided opportunities to examine VZV neuropathobiology and has shown the importance of intrinsic and innate responses that modulate VZV infection in vivo and in the absence of an adaptive immune response, which SCID mice lack. Using these tools to investigate VZV pathogenesis has provided insight into the clinical manifestations of varicella, herpes zoster and VZV-associated neurologic sequelae.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85017058573&origin=inward; http://dx.doi.org/10.1007/978-3-319-33189-8_5; http://link.springer.com/10.1007/978-3-319-33189-8_5; https://dx.doi.org/10.1007/978-3-319-33189-8_5; https://link.springer.com/chapter/10.1007/978-3-319-33189-8_5
Springer Science and Business Media LLC
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