Analysis of HTLV-I infection mechanisms using cell-free virus

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1) We showed that the expression of HSC70 enhanced HTLV-I-induced cell fusion but did not affect the efficiency of cell-free HTLV-I plating, suggesting that HSC7O binds to HTLV-I but is not its receptor.2) When 8C cells expressing Tax of HTLV-I were infected with cell-free HTLV-I, numerous syncytia were formed in these cells and production of progeny HTLV-I was detected in culture supernatants.3) Pseudotype virus, namely, chimeric vesicular stomatitis virus (VSV) containing GFP gene that bears envelope proteins of HTLV-I, was formed efficiently when HTLV-I-producing cells were infected with chimeric VSV.4) We found that HTLV-I was highly sensitive to ultraviolet light irradiation and that it was not so stable at 37℃, as compared with bovine leukemia virus (BLV).5) When human synovial cells were infected with HTLV-I or BLV, both viruses were detected shortly after infection. The cells infected with BLV but not HTLV-I grew more than one year in tissue culture.6) One of oligopeptides encompassing gp21 inhibited HTLV-I infection at a step after virus adsorption.7) Sera of HTLV-I-infected subjects inhibited HTLV-I infection in vitro after virus adsorption step.8) HTLV-I produced from cells treated with glycosylation inhibitors, especially inhibitors at early steps of glycosylation showed reduced infectivities. In contrast, sialidase enhanced its infectivity.9) Injection of human osetosarcoma cells infected with HTLV-I or transduced with tax into nude mice induced rapid tumor formation, splenomegaly and neutrophilia. G-CSF or GM-CSF was detected in their sera at high levels.