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The presence of tat protein or tumor necrosis factor alpha is critical for herpes simplex virus type 1-induced expression of human immunodeficiency virus type 1.
J Virol. 1994 Mar; 68(3):1324-33.JV

Abstract

Tat-independent transcription of human immunodeficiency virus type 1 (HIV-1) plays an important role in virus life cycle before biologically significant levels of Tat protein have been accumulated. Using a latently infected T-cell line containing an integrated Tat-defective HIV-1 provirus, we examined whether factors known to up-regulate the HIV-1 expression in vitro can replace the requirement for a functional Tat protein and induce the expression of the Tat-defective HIV-1 provirus. Both tumor necrosis factor alpha (TNF-alpha) and herpes simplex virus type 1 (HSV-1) infection stimulated transcription of the Tat-defective HIV-1 provirus to comparable levels, but in HSV-1-infected cells, the cytoplasmic HIV-1 transcripts were not efficiently translated in the absence of Tat protein and were excluded from the large polysomes. However, HSV-1 infection did not affect the distribution of cellular gamma-actin RNA or 28S RNA in the polysomal fractions. The translational block of HIV-1 RNA was not mediated by the virion-associated host cell shutoff protein (vhs); dissociation of HIV-1 transcripts from the polysomes and inefficient translation was also observed in cells infected with the vhs-defective mutant of HSV-1 (vhs-1). Overexpression of Rev protein did not rescue the synthesis of HIV-1 proteins in these cells; however, the observed inhibition of HIV-1 RNA translation was efficiently overcome in the presence of Tat protein or TNF-alpha. These findings suggest that, in contrast to TNF-alpha, HSV-1 infection is not able to induce a full cycle of HIV-1 replication and that cytokines and Tat have a critical role in the activation of HIV-1 provirus by HSV-1.

Authors+Show Affiliations

Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8107197

Citation

Popik, W, and P M. Pitha. "The Presence of Tat Protein or Tumor Necrosis Factor Alpha Is Critical for Herpes Simplex Virus Type 1-induced Expression of Human Immunodeficiency Virus Type 1." Journal of Virology, vol. 68, no. 3, 1994, pp. 1324-33.
Popik W, Pitha PM. The presence of tat protein or tumor necrosis factor alpha is critical for herpes simplex virus type 1-induced expression of human immunodeficiency virus type 1. J Virol. 1994;68(3):1324-33.
Popik, W., & Pitha, P. M. (1994). The presence of tat protein or tumor necrosis factor alpha is critical for herpes simplex virus type 1-induced expression of human immunodeficiency virus type 1. Journal of Virology, 68(3), 1324-33.
Popik W, Pitha PM. The Presence of Tat Protein or Tumor Necrosis Factor Alpha Is Critical for Herpes Simplex Virus Type 1-induced Expression of Human Immunodeficiency Virus Type 1. J Virol. 1994;68(3):1324-33. PubMed PMID: 8107197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The presence of tat protein or tumor necrosis factor alpha is critical for herpes simplex virus type 1-induced expression of human immunodeficiency virus type 1. AU - Popik,W, AU - Pitha,P M, PY - 1994/3/1/pubmed PY - 1994/3/1/medline PY - 1994/3/1/entrez SP - 1324 EP - 33 JF - Journal of virology JO - J Virol VL - 68 IS - 3 N2 - Tat-independent transcription of human immunodeficiency virus type 1 (HIV-1) plays an important role in virus life cycle before biologically significant levels of Tat protein have been accumulated. Using a latently infected T-cell line containing an integrated Tat-defective HIV-1 provirus, we examined whether factors known to up-regulate the HIV-1 expression in vitro can replace the requirement for a functional Tat protein and induce the expression of the Tat-defective HIV-1 provirus. Both tumor necrosis factor alpha (TNF-alpha) and herpes simplex virus type 1 (HSV-1) infection stimulated transcription of the Tat-defective HIV-1 provirus to comparable levels, but in HSV-1-infected cells, the cytoplasmic HIV-1 transcripts were not efficiently translated in the absence of Tat protein and were excluded from the large polysomes. However, HSV-1 infection did not affect the distribution of cellular gamma-actin RNA or 28S RNA in the polysomal fractions. The translational block of HIV-1 RNA was not mediated by the virion-associated host cell shutoff protein (vhs); dissociation of HIV-1 transcripts from the polysomes and inefficient translation was also observed in cells infected with the vhs-defective mutant of HSV-1 (vhs-1). Overexpression of Rev protein did not rescue the synthesis of HIV-1 proteins in these cells; however, the observed inhibition of HIV-1 RNA translation was efficiently overcome in the presence of Tat protein or TNF-alpha. These findings suggest that, in contrast to TNF-alpha, HSV-1 infection is not able to induce a full cycle of HIV-1 replication and that cytokines and Tat have a critical role in the activation of HIV-1 provirus by HSV-1. SN - 0022-538X UR - https://www.unboundmedicine.com/medline/citation/8107197/The_presence_of_tat_protein_or_tumor_necrosis_factor_alpha_is_critical_for_herpes_simplex_virus_type_1_induced_expression_of_human_immunodeficiency_virus_type_1_ L2 - http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=8107197 DB - PRIME DP - Unbound Medicine ER -