*4.7. HIV*

Circulating LF plasma levels in HIV-1-infected patients was significantly decreased compared to non-infected patients [104], suggesting an important role for LF during HIV-1 infection and disease progression. Experiments assessing the role of LF in HIV-1 infection in peripheral blood mononuclear cells revealed LF (IC50 = 9.6 μM) as a potent inhibitor of six clinical isolates of HIV-1 in a dose-dependent manner upon treatment of cells prior to infection [105]. Additionally, synergistic effects of human and bovine LF were assessed in combination with zidovudine, which also demonstrated a dose-dependent inhibition [105]. Bovine LF inhibited the HIV-1 entry process by binding to the viral envelope, and HIV-1 variants resistant to LF exhibit mutations in the viral envelope protein [106]. Bovine LF was found to be a more potent inhibitor than human LF in preventing dendritic cell-mediated HIV-1 transmission between cells by directly and strongly binding to DC-SIGN, a receptor molecule on dendritic cells that mediates HIV-1 internalization [106].

In pediatric HIV-1 infections, LF enhanced responses to antiretroviral therapy by decreasing plasma viral load and modulating the immune system [107,108]. LF treatment alone increased CD4+ cell counts, but a more significant increase was observed when LF was combined with antiretroviral therapy [107]. Result suggested that no HIV-1-related symptoms were evident for the duration of the experiments. However, large-scale studies are required in order to further assess LF's therapeutic potential against HIV.
