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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.1019)
Hurwitz AA, Hatch WC, Lyman WD, Hatcher VB, Berman JW; Albert Einstein Coll. Med., NY, NY, USA
OBJECTIVE: To test the hypothesis that endothelial cells can be infected by HIV-1.
METHODS: Early passage human umbilical vein endothelial (HUVE) cells were transfected with a full-length CD4 cDNA and a selectable neomycin-resistance marker (CD4+EC). CD4+EC and nontransfected control HUVE were tested for CD4 expression by nucleic acid hybridization and flow cytometry. CD4+EC and nontransfected HUVE (CD4-EC) were cultured with HIVIIIb. Infection of HUVE by HIV-1 was determined by measuring reverse transcriptase (RT) activity and viral antigen (p24) concentration, and by in situ hybridization using a full-length cDNA probe.
RESULTS: Transfected HUVE both contained and expressed the CD4 gene as determined by Southern and Northern blotting. Flow cytometry confirmed that approximately 20% of CD4+EC expressed surface CD4. Supernatants of CD4+EC exposed to virus contained more HIV-1 RT and p24 than CD4-EC supernatants. No HIV-1 was detected in any HUVE culture by in situ hybridization.
DISCUSSION AND CONCLUSIONS: Although HIVIIIb bound to CD4+EC, these cells were not productively infected. This may have been due to viral cytotoxicity for HUVE, an endothelial cell regulatory mechanism, or to the HIV-1 isolate tested. However, these data do not exclude the possibility of a latent infection nor do they eliminate the expectation that HIV infection of endothelial cells may occur via CD4-independent mechanisms in vitro or in vivo. The present findings are consistent with the minimal evidence for HIV-1 infection of endothelium in vivo, either in the central nervous system or in the systemic circulation.
Copyright © 1991 - International AIDS Society (IAS). Reproduction of this abstract (other than one copy for personal reference) must be cleared through the IAS.