[Studying the course of HIV-1 infection in cell culture]

The hallmark of AIDS is the gradual loss of CD4+ T-lymphocytes, in spite of their infection in low ratio. The pathomechanism is hardly known, therefore, the production of HIV-1 and certain aspects of cell death were studied. Infectivity was decreased by the acidification of culture media. C8166 cells transformed by HTLV-I and exhibiting features of both immature T lymphocytes and myeloid cells, produced transient protoplasmic surface extrusions, similar to the hairy cell leukemia. These can have a role in the direct cell-to-cell spread of HIV-1. Polarization of nuclei and cell organelles as well as sites of virus budding during syncytium formation resembled the directed lymphokine secretion. Both cell membrane and intravacuolar buddings were characteristic. Abnormal virus particles also were seen. Certain morphological signs resembled apoptosis. Fibroblast cultures in the presence of HIV-1 infected lymphoid cells were arrested in growth and underwent cell death without syncytium formation. The results draw attention to the faster development of AIDS in the case of HIV-1 infection of precursor immune cells. Double infection by HTLV and HIV-1 can result in atypical leukemias.