HIV TYPE-1 GROWN ON INTERFERON GAMMA-TREATED U937 CELLS SHOWS SELECTIVE INCREASE IN VIRION-ASSOCIATED INTERCELLULAR-ADHESION MOLECULE-1 ANDHLA-DR AND ENHANCED INFECTIVITY FOR CD4-NEGATIVE CELLS

Citation
C. Castilletti et al., HIV TYPE-1 GROWN ON INTERFERON GAMMA-TREATED U937 CELLS SHOWS SELECTIVE INCREASE IN VIRION-ASSOCIATED INTERCELLULAR-ADHESION MOLECULE-1 ANDHLA-DR AND ENHANCED INFECTIVITY FOR CD4-NEGATIVE CELLS, AIDS research and human retroviruses, 11(5), 1995, pp. 547-553
Citations number
33
Categorie Soggetti
Immunology,"Infectious Diseases
ISSN journal
08892229
Volume
11
Issue
5
Year of publication
1995
Pages
547 - 553
Database
ISI
SICI code
0889-2229(1995)11:5<547:HTGOIG>2.0.ZU;2-A
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 fro m infected cells, These virion-associated molecules can be involved in the adsorption to susceptible cells displaying the corresponding coun terligands, A number of cytokines have been shown to upregulate the ce llular expression of adhesion molecules, such as ICAM-1 and HLA-DR. In this study we investigated the effects of IFN-gamma on the incorporat ion of ICAM-1, LFA-1, and HLA-DR into mature HIV-1 progeny from chroni cally infected cells, The ability of such virus progeny to infect eith er 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, T he same modifications were also observed on virus progeny, because spe cific MAbs to ICAM-1 and HLA-DR captured infectious HIV-1 from IFN-tre ated cells with higher efficiency as compared to virus from control ce lls, 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 infec tivity was basically unchanged for CD4-positive cells. Our results sug gest that cytokines, as well as other soluble factors, may expand the host cell range of HIV-1, possibly through modifications of the cell-d erived surface molecules on the virions, These could, in turn, act as alternative or additional ligands for virus attachment to host cells t hat display the corresponding counterreceptor(s).