Tracing complement-retroviral interactions from mucosal surfaces to the lymphatic tissue.

During (nearly) all steps in retroviral pathogenesis, viruses are confronted with complement and complement receptor (CR)-positive cells. As all of the retroviruses tested so far activate the complement system, members of this virus family have adapted different protection mechanisms to keep complement activation under the threshold necessary to avoid complement-mediated lysis. As a consequence of complement activation, retroviruses are covered with complement proteins and thus provide additional ligands to interact with CR-expressing cells. This review discusses the complex complement-retroviral interactions and follows the fate of the virus on its way to the lymphatic tissue.

Changes in HIV-specific antibody responses and neutralization titers in patients under ART.

In this study, we tested for antibody reactivities against gp120 and gp41-derived peptides, recombinant gp160, gp41 and tat in HIV-positive sera under antiretroviral therapy (ART) and determined their neutralization capacity. As a baseline, sera from patients in stage A, B and C of the disease, long term non-progressors (LNPs) and HIV-negative individuals were included. Compared to LNPs or sera from patients in group A, the reactivity of sera in stage B or C against gp120-derived peptides was reduced parallel to disease progression. Reactivity of these samples was compared with sera of patients under ART. Parallel to the decrease of viral load, the reactivity against gp120 and gp41-derived epitopes, recombinant gp160 and gp41 or the native gp120/41 complex was significantly reduced. Antibody-mediated neutralization of HIV-1 was detectable prior to ART but revealed substantial decreases coupled with progression of therapy. Responses to recombinant tat dropped after three months of therapy, increased however at later time points to initial levels. These data indicate that in parallel to the decrease in viral load and antibodies against gp120, the neutralization capacity of sera under ART is reduced, and can not be compensated by an increase in tat-specific antibodies.