Interferons have limited direct antiviral effects on HTLV-III replication in chronically infected cells, but their effects are enhanced by cell-mediated mechanisms involving normal peripheral blood mononuclear cells.
Augmented IFN effects via immune cells suggest synergy in HIV; leaves open therapeutic relevance pending human studies.
The replication of the human T lymphotropic retrovirus HTLV-III in persistently infected cells is relatively insensitive to the direct antiviral action of human interferon-alpha or -gamma (IFN-alpha or -gamma), showing only a two- to threefold reduction of HTLV-III, even though the host cells are very sensitive to IFN, as shown by vesicular stomatitis virus (VSV)-yield reduction assay (4-5 log reduction of VSV). However, IFN anticellular activity is strongly enhanced in the presence of normal peripheral blood mononuclear cells, suggesting a cell-mediated effect of IFNs.
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Dolei et al. (1986) studied this question.
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