HIV type 1 grown on interferon gamma-treated U937 cells shows selective increase in virion-associated intercellular adhesion molecule 1 and HLA-DR and enhanced infectivity for CD4-negative cells.

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HIV type 1 grown on interferon gamma-treated U937 cells shows selective increase in virion-associated intercellular adhesion molecule 1 and HLA-DR and enhanced infectivity for CD4-negative cells.

AIDS Res Hum Retroviruses. 1995 May;11(5):547-53. Unique Identifier : AIDSLINE MED/96093889
Castilletti C; Capobianchi MR; Fais S; Abbate I; Ficociello B; Ameglio F; Cordiali Fei P; Santini SM; Dianzani F; Institute of Virology, University La Sapienza, Rome.

Abstract: Cellular adhesion molecules, such as ICAM-1, -2, and -3; LFA-1; and HLA class I and II are incorporated into HIV-1 virions during budding from infected cells. These virion-associated molecules can be involved in the adsorption to susceptible cells displaying the corresponding counterligands. A number of cytokines have been shown to upregulate the cellular expression of adhesion molecules, such as ICAM-1 and HLA-DR. In this study we investigated the effects of IFN-gamma on the incorporation of ICAM-1, LFA-1, and HLA-DR into mature HIV-1 progeny from chronically infected cells. The ability of such virus progeny to infect either CD4-positive or -negative cells was also investigated. The results indicate that IFN-gamma stimulates the expression of ICAM-1 and of HLA-DR on HIV-1-infected cells, whereas LFA-1 expression is unaffected. The same modifications were also observed on virus progeny, because specific MAbs to ICAM-1 and HLA-DR captured infectious HIV-1 from IFN-treated cells with higher efficiency as compared to virus from control cells, whereas virus binding to anti LFA-1 MAb was unchanged. Moreover, the HIV-1 progeny released from IFN-treated cells showed an increased ability to bind to and to infect CD4-negative cells, whereas the infectivity was basically unchanged for CD4-positive cells. Our results suggest that cytokines, as well as other soluble factors, may expand the host cell range of HIV-1, possibly through modifications of the cell-derived surface molecules on the virions.(ABSTRACT TRUNCATED AT 250 WORDS)

Keywords: Antigens, CD4 Cell Line Human HIV-1/METABOLISM/*PATHOGENICITY HLA-DR Antigens/*METABOLISM Intercellular Adhesion Molecule-1/*METABOLISM Interferon Type II/*PHARMACOLOGY Lymphocyte Function-Associated Antigen-1/*METABOLISM Monocytes/METABOLISM/VIROLOGY Support, Non-U.S. Gov't JOURNAL ARTICLE
960228
M9621039

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