Abstract
The Herpes Simplex Virus Neurovirulence Factor γ34.5: Revealing Virus-Host Interactions.
Highlights
Herpes simplex virus (HSV) is a ubiquitous human pathogen that causes a wide spectrum of disease, ranging from asymptomatic viral shedding to lethal encephalitis and disseminated disease [1,2]
HSV γ34.5 is required for full virulence in the murine brain [6,7]; recent evidence suggests that γ34.5 may function differently in newborn models of HSV disease compared to the adult [8]
We provide a brief overview of the multiple host responses modulated by γ34.5 for successful HSV replication in the nervous system and discuss recent evidence that expands the role of γ34.5 to promote pathogenesis in several different tissue-types and across different developmental ages of the host
Summary
Herpes simplex virus (HSV) is a ubiquitous human pathogen that causes a wide spectrum of disease, ranging from asymptomatic viral shedding to lethal encephalitis and disseminated disease [1,2]. To successfully replicate in the host nervous system, HSV encodes several viral proteins to counter the host innate response to infection.
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