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-γ 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-γ 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. These could, in turn, act as alternative or additional ligands for virus attachment to hast cells that display the corresponding counterreceptor(s).
| Original language | English |
|---|---|
| Pages (from-to) | 547-553 |
| Number of pages | 7 |
| Journal | AIDS Research and Human Retroviruses |
| Volume | 11 |
| Issue number | 5 |
| Publication status | Published - 1995 |
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ASJC Scopus subject areas
- Immunology
- Virology
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HIV type 1 grown on interferon γ-treated U937 cells shows selective increase in virion-associated intercellular adhesion molecule 1 and HLA-DR and enhanced infectivity for CD4-negative cells. / Castilletti, C.; Capobianchi, M. R.; Fais, S.; Abbate, I.; Ficociello, B.; Ameglio, F.; Fei, P. C.; Santini, S. M.; Dianzani, F.
In: AIDS Research and Human Retroviruses, Vol. 11, No. 5, 1995, p. 547-553.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - HIV type 1 grown on interferon γ-treated U937 cells shows selective increase in virion-associated intercellular adhesion molecule 1 and HLA-DR and enhanced infectivity for CD4-negative cells
AU - Castilletti, C.
AU - Capobianchi, M. R.
AU - Fais, S.
AU - Abbate, I.
AU - Ficociello, B.
AU - Ameglio, F.
AU - Fei, P. C.
AU - Santini, S. M.
AU - Dianzani, F.
PY - 1995
Y1 - 1995
N2 - 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-γ 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-γ 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. These could, in turn, act as alternative or additional ligands for virus attachment to hast cells that display the corresponding counterreceptor(s).
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-γ 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-γ 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. These could, in turn, act as alternative or additional ligands for virus attachment to hast cells that display the corresponding counterreceptor(s).
UR - http://www.scopus.com/inward/record.url?scp=0028979183&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028979183&partnerID=8YFLogxK
M3 - Article
C2 - 7576910
AN - SCOPUS:0028979183
VL - 11
SP - 547
EP - 553
JO - AIDS Research and Human Retroviruses
JF - AIDS Research and Human Retroviruses
SN - 0889-2229
IS - 5
ER -