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7th International AIDS ConferenceFlorence, Italy — June 16-21, 1991 |
Int Conf AIDS 1991 Jun 16-21; 7:96 (abstract no. M.A.1018)
Lazdins J, Alteri E, Woods-Cook K, Klimkait T, Cox D, Bilbe G, Cerletti N, McMaster G; CIBA-GEIGY Ltd. Basel CH 4002
OBJECTIVE: Evaluation of the role of TGF-Beta on HIV-1 replication in blood derived macrophages (M0).
METHODS: Monocytes were isolated by leukapheresis and purified by elutriation. After differentiation M0 were infected with HIV-1 ADA (monocytotropic) IIIB, LAV or Z-84 (lymphocytotropic). Infection was evaluated by supernatant p24 ag., RT activity, morphology and immunoblot analysis.
RESULTS: Infection of M0 with ADA shows an enhanced viral replication in the presence of TGF-Beta 1 or 2. When M0 were infected with IIIB, LAV, Z-84 no p24 or RT was detected in cell supernatants; however, immunoblots show a p55 band. When infection with these isolates is performed in the presence of TGF-Beta a dose dependent virus production was demonstrated. The virus that emerged retained its original cell tropism.
DISCUSSION AND CONCLUSIONS: TGF-Beta, a factor produced at the site of injury, facilitates virus replication in M0, independent of the viral tropism. This effect is not due to apparent changes in cell phenotype. This effect was not seen with other cytokines. Since M0 can produce TGF-Beta this molecule could play a critical role in the establishment of infection as well as progression of disease. Furthermore this effect of TGF-Beta could play an important role in infection in tissues where M0 are important cell targets, i.e.: brain.
Copyright © 1991 - International AIDS Society (IAS). Reproduction of this abstract (other than one copy for personal reference) must be cleared through the IAS.