Varicella-Zoster Virus (VZV) Virion-Associated Transactivator Open Reading Frame 62 Protein Enhances the Infectivity of VZV DNA

Moriuchi, Masako; Moriuchi, Hiroyuki; Straus, Stephen E.; Cohen, Jeffrey I.

doi:10.1006/viro.1994.1190

Cited by 100 publications

(109 citation statements)

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“…Plasmids pGL-RANTES, pGL-CCR5, and pGL-CXCR4 are luciferase reporter constructs for the promoter regions of RANTES, CCR5, and CXCR4, respectively (38)(39)(40). Blood monocytes were plated on 60-mm diameter tissue culture plates, and 3-5 d later, the cells were transfected with the above-mentioned plasmids by a modified calcium phosphate method (41). The transfected cell lysates were tested for luciferase activity 3 d later, as described above.…”

Section: Methodsmentioning

confidence: 99%

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Moriuchi

Moriuchi²,

Turner³

et al. 1998

J. Clin. Invest.

106

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Microbial coinfections variably influence HIV-1 infection through immune activation or direct interaction of microorganisms with HIV-1 or its target cells. In this study, we investigated whether exposure of macrophages to bacterial products impacts the susceptibility of these cells to HIV-1 of different cellular tropisms.We demonstrate that (1) macrophages exposed to bacterial cell wall components such as lipopolysaccharide (

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Section: Methodsmentioning

confidence: 99%

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Moriuchi

Moriuchi²,

Turner³

et al. 1998

J. Clin. Invest.

106

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“…Cosmids were linearized with NotI or MstII. One lag of cosmids VZV NotI A-14S, NotI BD and MstII B, 0"5 lag of cosmid VZV MstII A, 0.05 tag of plasmid pCMV62 and 2 lag of sheared salmon sperm DNA were used to transfect human melanoma cells in 60 mm dishes using the calcium phosphate procedure (Moriuchi et al, 1993). Six days after transfection, the cells were passaged into 75 cm 2 flasks.…”

Section: Methodsmentioning

confidence: 99%

Absence of Varicella-zoster Virus (VZV) Glycoprotein V Does not Alter Growth of VZV in vitro or Sensitivity to Heparin

Cohen

Seidel

1994

Journal of General Virology

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Varicella-zoster virus (VZV) encodes at least five glycoproteins, gpI to gpV. VZV gpV, M,. 100K to 110K, is the product of VZV open reading frame (ORF) 14. VZV gpV is homologous to herpes simplex virus gC and pseudorabies virus gIII. To determine whether gpV is required for viral replication, we inserted a stop codon after the fifteenth codon of the ORF14 gene in a cosmid containing the gene. Transfection of human melanoma cells with the cosmid containing the mutant ORF14 gene and three other cosmids resulted in the production of infectious VZV. Immunoprecipitation indicated that the mutant virus did not express gpV. VZV that did not express gpV grew at the same rate as parental virus and was inhibited by heparin to a similar extent. The pattern of inhibition by heparin of the gpV mutant was similar to that reported for a herpes simplex virus mutant that does not contain gC, but different from that described for a pseudorabies virus mutant devoid of gIII. These results indicate that VZV gpV is not required for viral replication in vitro.

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“…VZV encodes orthologs of both ICP0 and U S 3 kinase, termed ORF61p and ORF66p, respectively (34,47). Like ICP0, ORF61p is a transcriptional activator and it enhances infectivity of viral DNA and targets ND10 components (29,34,35). In addition, a recent study suggests that ORF61p may have a role in inhibiting HDAC activity, further confirming the orthologous nature of these proteins (51).…”

mentioning

confidence: 92%

Histone Deacetylases 1 and 2 Are Phosphorylated at Novel Sites during Varicella-Zoster Virus Infection

Walters

Erazo

Kinchington³

et al. 2009

J Virol

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ORF66p, a virion-associated varicella-zoster virus (VZV) protein, is a member of a conserved Alphaherpesvirinae kinase family with homology to herpes simplex virus U S 3 kinase. Expression of ORF66p in cells infected with VZV or an adenovirus expressing only ORF66p results in hyperphosphorylation of histone deacetylase 1 (HDAC1) and HDAC2. Mapping studies reveal that phosphorylation is at a unique conserved Ser residue in the C terminus of both HDACs. This modification requires an active kinase domain in ORF66p, as neither protein is phosphorylated in cells infected with VZV lacking kinase activity. However, hyperphosphorylation appears to occur indirectly, as within the context of in vitro kinase reactions, purified ORF66p phosphorylates a peptide derived from ORF62p, a known substrate, but does not phosphorylate HDAC. These results support a model where ORF66p is necessary but not sufficient to effect hyperphosphorylation of HDAC1 and HDAC2.

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Varicella-Zoster Virus (VZV) Virion-Associated Transactivator Open Reading Frame 62 Protein Enhances the Infectivity of VZV DNA

Cited by 100 publications

References 0 publications

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Exposure to bacterial products renders macrophages highly susceptible to T-tropic HIV-1.

Absence of Varicella-zoster Virus (VZV) Glycoprotein V Does not Alter Growth of VZV in vitro or Sensitivity to Heparin

Histone Deacetylases 1 and 2 Are Phosphorylated at Novel Sites during Varicella-Zoster Virus Infection

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