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Cooperation between herpes simplex virus type 1-encoded ICP0 and Tat to support transcription of human immunodeficiency virus type 1 long terminal repeat in vivo can occur in the absence of the TAR binding site.
J Virol. 1996 Oct; 70(10):6937-46.JV

Abstract

Expression of human immunodeficiency virus type 1 (HIV-1) provirus can be stimulated by herpes simplex virus type 1 (HSV-1) infection; the stimulation occurs at the level of transcriptional activation of the HIV long terminal repeat (LTR) and is mediated by both cellular and HSV-1-encoded transactivators. We have shown in this study that HSV-1 immediate-early gene ICP0 cooperates effectively with the HIV-1-encoded transactivator, Tat, in the stimulation of HIV-1 LTR-directed transcription. The cooperation between ICP0 and Tat is specific for the HIV-1 LTR and was not observed with other promoters (e.g., ICP0) that can be transactivated by ICP0 but not by Tat. Analyses of HIV-1 LTR deletion mutants have shown that ICP0 not only transactivates an HIV-1 LTR mutant that is unresponsive to NF-kappaB and Tat-mediated transactivation, such as the HIV-1 LTR with the enhancer deleted (-83 LTR) and TAR deleted (+20 to +81), but also restores responsiveness to Tat. ICP0 also showed cooperation with Gal4-Tat fusion protein-mediated transactivation of Gal4-HIV-1 LTR with TAR deleted. Enhancement of the transcriptional activation of ICP0 by Tat requires both the cysteine-rich and core domains of Tat and is inhibited by RO5-3335. ICP0 stimulates transcription of not only the HIV-1 LTR but also the TAR-defective HIV-1 provirus. We suggest that ICP0 can (i) recruit Tat to the vicinity of the HIV-1 promoter, thereby providing an alternative binding site for Tat, and (ii) substitute for the enhancer-binding proteins that are required for efficient Tat transactivation in T cells.

Authors+Show Affiliations

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

8794337

Citation

Schafer, S L., et al. "Cooperation Between Herpes Simplex Virus Type 1-encoded ICP0 and Tat to Support Transcription of Human Immunodeficiency Virus Type 1 Long Terminal Repeat in Vivo Can Occur in the Absence of the TAR Binding Site." Journal of Virology, vol. 70, no. 10, 1996, pp. 6937-46.
Schafer SL, Vlach J, Pitha PM. Cooperation between herpes simplex virus type 1-encoded ICP0 and Tat to support transcription of human immunodeficiency virus type 1 long terminal repeat in vivo can occur in the absence of the TAR binding site. J Virol. 1996;70(10):6937-46.
Schafer, S. L., Vlach, J., & Pitha, P. M. (1996). Cooperation between herpes simplex virus type 1-encoded ICP0 and Tat to support transcription of human immunodeficiency virus type 1 long terminal repeat in vivo can occur in the absence of the TAR binding site. Journal of Virology, 70(10), 6937-46.
Schafer SL, Vlach J, Pitha PM. Cooperation Between Herpes Simplex Virus Type 1-encoded ICP0 and Tat to Support Transcription of Human Immunodeficiency Virus Type 1 Long Terminal Repeat in Vivo Can Occur in the Absence of the TAR Binding Site. J Virol. 1996;70(10):6937-46. PubMed PMID: 8794337.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cooperation between herpes simplex virus type 1-encoded ICP0 and Tat to support transcription of human immunodeficiency virus type 1 long terminal repeat in vivo can occur in the absence of the TAR binding site. AU - Schafer,S L, AU - Vlach,J, AU - Pitha,P M, PY - 1996/10/1/pubmed PY - 1996/10/1/medline PY - 1996/10/1/entrez SP - 6937 EP - 46 JF - Journal of virology JO - J Virol VL - 70 IS - 10 N2 - Expression of human immunodeficiency virus type 1 (HIV-1) provirus can be stimulated by herpes simplex virus type 1 (HSV-1) infection; the stimulation occurs at the level of transcriptional activation of the HIV long terminal repeat (LTR) and is mediated by both cellular and HSV-1-encoded transactivators. We have shown in this study that HSV-1 immediate-early gene ICP0 cooperates effectively with the HIV-1-encoded transactivator, Tat, in the stimulation of HIV-1 LTR-directed transcription. The cooperation between ICP0 and Tat is specific for the HIV-1 LTR and was not observed with other promoters (e.g., ICP0) that can be transactivated by ICP0 but not by Tat. Analyses of HIV-1 LTR deletion mutants have shown that ICP0 not only transactivates an HIV-1 LTR mutant that is unresponsive to NF-kappaB and Tat-mediated transactivation, such as the HIV-1 LTR with the enhancer deleted (-83 LTR) and TAR deleted (+20 to +81), but also restores responsiveness to Tat. ICP0 also showed cooperation with Gal4-Tat fusion protein-mediated transactivation of Gal4-HIV-1 LTR with TAR deleted. Enhancement of the transcriptional activation of ICP0 by Tat requires both the cysteine-rich and core domains of Tat and is inhibited by RO5-3335. ICP0 stimulates transcription of not only the HIV-1 LTR but also the TAR-defective HIV-1 provirus. We suggest that ICP0 can (i) recruit Tat to the vicinity of the HIV-1 promoter, thereby providing an alternative binding site for Tat, and (ii) substitute for the enhancer-binding proteins that are required for efficient Tat transactivation in T cells. SN - 0022-538X UR - https://www.unboundmedicine.com/medline/citation/8794337/Cooperation_between_herpes_simplex_virus_type_1_encoded_ICP0_and_Tat_to_support_transcription_of_human_immunodeficiency_virus_type_1_long_terminal_repeat_in_vivo_can_occur_in_the_absence_of_the_TAR_binding_site_ L2 - http://jvi.asm.org/cgi/pmidlookup?view=long&pmid=8794337 DB - PRIME DP - Unbound Medicine ER -