INVOLVEMENT OF ALPHA-INTERFERON IN HIV-1 INDUCED IMMUNOSUPPRESSION - A POTENTIAL TARGET FOR AIDS PROPHYLAXIS AND TREATMENT

Citation
A. Lachgar et B. Bizzini, INVOLVEMENT OF ALPHA-INTERFERON IN HIV-1 INDUCED IMMUNOSUPPRESSION - A POTENTIAL TARGET FOR AIDS PROPHYLAXIS AND TREATMENT, Biomedicine & pharmacotherapy, 48(2), 1994, pp. 73-77
Citations number
16
Categorie Soggetti
Pharmacology & Pharmacy","Medicine, Research & Experimental
ISSN journal
07533322
Volume
48
Issue
2
Year of publication
1994
Pages
73 - 77
Database
ISI
SICI code
0753-3322(1994)48:2<73:IOAIHI>2.0.ZU;2-P
Abstract
Since the immune system is impaired in the course of HIV-infection, th e purpose of any AIDS vaccine therapy should be the restoration in the patient of an adequate immunocompetence to enable him to respond to t he antigenic stimulus represented by the virus. In the present investi gation we have shown the antiproliferative action on activated T-cells in culture of: sera taken from HIV-infected, but not seronegative ind ividuals; T lymphocytes taken from seronegative subjects and infected in vitro with HIV but not non infected cells; native alpha-IFN and the time-dependent inactivation of this activity by formaldehyde treatmen t of alpha-IFN. Thus is confirmed the major contribution provided by a lpha-IFN to the immunosuppression occurring in the course of HIV-infec tion. These results also strongly support the new AIDS vaccine therapy strategy based on the administration to HIV-infected patients of inac tivated, but still immunogenic alpha-IFN. To the alpha-IFN treatment c ould also be combined the administration of fixed autologous suppressi ve cells. The induction of gamma-IFN in addition to alpha-IFN producti on by stimulation of cells from healthy donors with gp120 should encou rage the use of a vaccine combining both inactivated alpha-IFN and gam ma-IFN. On the other hand, the IL-12 cytokine with its potential to re store compromised cell-mediated functions associated with HIV infectio n should also be a valuable adjuvant treatment.