Tags

Type your tag names separated by a space and hit enter

Inhibition by interferon of herpes simplex virus type 1-activated transcription of tat-defective provirus.
Proc Natl Acad Sci U S A. 1991 Nov 01; 88(21):9573-7.PN

Abstract

The herpes simplex virus type 1 (HSV-1)-mediated transactivation of human immunodeficiency virus type 1 (HIV-1) provirus was studied in cell lines containing either integrated tat-defective HIV-1 provirus (HNHIVdt4 cells) or the tat-defective HIV-1 provirus, and a plasmid in which the expression of human alpha 2 interferon (HuIFN-alpha 2) was under the control of the HIV-1 long terminal repeat (LTR) (HNHIV alpha 1 cells). In both cell lines, transcription of the HIV-1 provirus was below the limits of detection, but it could be induced effectively by transfection with a HIV-1 tat-expression plasmid. In HNHIV alpha 1 cells, HuIFN-alpha 2 was induced concomitantly with HIV-1 provirus, although these cells synthesized only low levels of IFN constitutively. In contrast, infections with HSV-1 activated transcription of HIV-1 provirus only in HNHIVdt4 cells but not in HNHIV alpha 1 cells. Similarly in a transient expression assay, HSV-1 up-regulated expression of a HIV LTR-CAT (chloramphenicol acetyltransferase gene) plasmid in HNHIVdt4 but not in HNHIV alpha 1 cells. No major differences could be detected in the expression of HSV-1 immediate-early (IE) genes IE175 and IE110 (which are essential for the activation of HIV-1 LTR) in HNHIVdt4 and HNHIV alpha 1 cells to account for the inability of HSV-1 to induce HIV-1 in HNHIV alpha 1 cells. However, major differences were observed in the binding pattern of NF-kappa B-specific nuclear proteins to the enhancer region of the HIV-1 LTR: whereas binding of the 45-kDa NF-kappa B-specific nuclear protein was detected in nuclear extracts from HNHIVdt4 cells, no protein binding was seen in extracts from HNHIV alpha 1 cells. These results suggest an alternate mechanism by which IFN may alter the expression of cellular and viral genes.

Authors+Show Affiliations

Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21205.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

1719535

Citation

Popik, W, and P M. Pitha. "Inhibition By Interferon of Herpes Simplex Virus Type 1-activated Transcription of Tat-defective Provirus." Proceedings of the National Academy of Sciences of the United States of America, vol. 88, no. 21, 1991, pp. 9573-7.
Popik W, Pitha PM. Inhibition by interferon of herpes simplex virus type 1-activated transcription of tat-defective provirus. Proc Natl Acad Sci U S A. 1991;88(21):9573-7.
Popik, W., & Pitha, P. M. (1991). Inhibition by interferon of herpes simplex virus type 1-activated transcription of tat-defective provirus. Proceedings of the National Academy of Sciences of the United States of America, 88(21), 9573-7.
Popik W, Pitha PM. Inhibition By Interferon of Herpes Simplex Virus Type 1-activated Transcription of Tat-defective Provirus. Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9573-7. PubMed PMID: 1719535.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition by interferon of herpes simplex virus type 1-activated transcription of tat-defective provirus. AU - Popik,W, AU - Pitha,P M, PY - 1991/11/1/pubmed PY - 1991/11/1/medline PY - 1991/11/1/entrez SP - 9573 EP - 7 JF - Proceedings of the National Academy of Sciences of the United States of America JO - Proc Natl Acad Sci U S A VL - 88 IS - 21 N2 - The herpes simplex virus type 1 (HSV-1)-mediated transactivation of human immunodeficiency virus type 1 (HIV-1) provirus was studied in cell lines containing either integrated tat-defective HIV-1 provirus (HNHIVdt4 cells) or the tat-defective HIV-1 provirus, and a plasmid in which the expression of human alpha 2 interferon (HuIFN-alpha 2) was under the control of the HIV-1 long terminal repeat (LTR) (HNHIV alpha 1 cells). In both cell lines, transcription of the HIV-1 provirus was below the limits of detection, but it could be induced effectively by transfection with a HIV-1 tat-expression plasmid. In HNHIV alpha 1 cells, HuIFN-alpha 2 was induced concomitantly with HIV-1 provirus, although these cells synthesized only low levels of IFN constitutively. In contrast, infections with HSV-1 activated transcription of HIV-1 provirus only in HNHIVdt4 cells but not in HNHIV alpha 1 cells. Similarly in a transient expression assay, HSV-1 up-regulated expression of a HIV LTR-CAT (chloramphenicol acetyltransferase gene) plasmid in HNHIVdt4 but not in HNHIV alpha 1 cells. No major differences could be detected in the expression of HSV-1 immediate-early (IE) genes IE175 and IE110 (which are essential for the activation of HIV-1 LTR) in HNHIVdt4 and HNHIV alpha 1 cells to account for the inability of HSV-1 to induce HIV-1 in HNHIV alpha 1 cells. However, major differences were observed in the binding pattern of NF-kappa B-specific nuclear proteins to the enhancer region of the HIV-1 LTR: whereas binding of the 45-kDa NF-kappa B-specific nuclear protein was detected in nuclear extracts from HNHIVdt4 cells, no protein binding was seen in extracts from HNHIV alpha 1 cells. These results suggest an alternate mechanism by which IFN may alter the expression of cellular and viral genes. SN - 0027-8424 UR - https://www.unboundmedicine.com/medline/citation/1719535/Inhibition_by_interferon_of_herpes_simplex_virus_type_1_activated_transcription_of_tat_defective_provirus_ L2 - http://www.pnas.org/cgi/pmidlookup?view=long&pmid=1719535 DB - PRIME DP - Unbound Medicine ER -