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June 25, 2004Journal of VirologyOpen Access

Replication of Herpes Simplex Virus 1 Depends on the γ 1 34.5 Functions That Facilitate Virus Response to Interferon and Egress in the Different Stages of Productive Infection

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Authors

XJXianghong JingChinese Academy of Medical Sciences & Peking Union Medical CollegeMCMelissa CervenyUniversity of Illinois ChicagoKYKui YangCenters for Disease Control and Prevention

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Jing et al. (2004) studied this question.

synapsesocial.com/papers/6a885e264c82be800eeb5bf5https://doi.org/10.1128/jvi.78.14.7653-7666.2004
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1The γ <sub>1</sub> 34.5 protein of herpes simplex virus 1 complexes with protein phosphatase 1α to dephosphorylate the α subunit of the eukaryotic translation initiation factor 2 and preclude the shutoff of protein synthesis by double-stranded RNA-activated protein kinase1997 · 756 citations
  2. 2Specific phenotypic restoration of an attenuated virus by knockout of a host resistance gene2000 · 230 citations
  3. 3The herpes simplex virus virulence factor ICP34.5 and the cellular protein MyD116 complex with proliferating cell nuclear antigen through the 63-amino-acid domain conserved in ICP34.5, MyD116, and GADD341997 · 98 citations
  4. 4The gamma 1(34.5) gene of herpes simplex virus 1 precludes neuroblastoma cells from triggering total shutoff of protein synthesis characteristic of programed cell death in neuronal cells.1992 · 396 citations
  5. 5Cell type and cell state determine differential in vitro growth of non-neurovirulent ICP34.5-negative herpes simplex virus types 1 and 21994 · 89 citations