       Document 1039
 DOCN  M9621039
 TI    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.
 DT    9602
 AU    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.
 SO    AIDS Res Hum Retroviruses. 1995 May;11(5):547-53. Unique Identifier :
       AIDSLINE MED/96093889
 AB    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)
 DE    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

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

