1679Interactions of the Herpes Simplex Virus γ34.5 Protein With Host Signaling Pathways Influence Central Nervous System Disease in Newborn Mice
نویسندگان
چکیده
Host Signaling Pathways Influence Central Nervous System Disease in Newborn Mice Douglas Wilcox; Diane Alexander PhD; David Leib, PhD; Bin He, PhD; William Muller, MD, PhD; Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL; Dartmouth Medical School, Lebanon, NH; University of Illinois, Chicago, Chicago, IL; Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL
منابع مشابه
The Herpes Simplex Virus Neurovirulence Factor γ34.5: Revealing Virus–Host Interactions
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]. These viruses belong to the neurotropic subfamily of α-herpesviruses, and after initial replication in epithelial cells, HSV enters sensory neurons to establish latency in neural ganglia. HSV can also pr...
متن کاملHSV targeting of the host phosphatase PP1α is required for disseminated disease in the neonate and contributes to pathogenesis in the brain.
Newborns are significantly more susceptible to severe disease after infection with herpes simplex virus (HSV) compared with adults, with differences in the host response implicated as a major factor. To understand host response differences between these age groups, we investigated the shutoff of protein synthesis by the host and the retargeting of host phosphatase PP1α by the HSV-1 protein γ34....
متن کاملPCR detection of thymidine kinase gen of latent herpes simplex Virus type 1 in mice trigeminal ganglia
Herpes simplex virus type 1 establishes a latent infection in the peripheral nervous system following primary infection. During latent infection, virus genome exhibit limited transcription, with the HSV LATs consistently detected in latency infected ganaglia. Following ocular infection viral latency develops in the trigeminal ganglia. In this study PCR has been used for detection of HSV-1 nuc...
متن کاملHerpes Simplex Virus γ34.5 Interferes with Autophagosome Maturation and Antigen Presentation in Dendritic Cells
The cellular autophagy response induced by herpes simplex virus 1 (HSV-1) is countered by the viral γ34.5 protein. γ34.5 modulates autophagy by binding to the host autophagy protein Beclin-1 and through this binding inhibits the formation of autophagosomes in fibroblasts and neurons. In contrast, in this study dendritic cells (DCs) infected with HSV-1 showed an accumulation of autophagosomes an...
متن کاملThe Effect of Herpes Simplex Virus Virion Host Shutoff Gene- a New Suicide Gene- on Tumor Cells
Background: The herpes simplex virus (HSV) UL41 gene product, virion host shutoff (Vhs) protein, mediates the rapid degradation of both viral and cellular mRNA. This ability suggests that Vhs protein can be used as a suicide gene in cancer gene therapy applications. The recent reports have shown that the degradation of cellular mRNA during herpes simplex infection is selective. RNA containing A...
متن کامل