We have shown that SEA parasite antigens and more specifically rП‰-1 can modulate HIV-1 infectivity with the potential to influence disease course in co-infected individuals. This inhibition associated again with a reduction in IFN-Оі and MIP-1ОІ expression, but additionally correlated with reduced CCR5 expression. We further show that DCs maturing under T mix conditions exposed to plant recombinant omega-1 protein (rП‰-1), which demonstrates similar functions to natural П‰-1, induced T-cell populations that were less sensitive for HIV-1 R5 infection (p<0.05), but not for X4 virus infection. The infection profile of T-cells infected with HIV-1 R5 was not associated with down-modulation of CCR5 cell surface expression. All T-cell populations induced by SEA exposed DCs demonstrate a reduced capacity to produce IFN-Оі and MIP-1ОІ. This was not observed for DCs exposed to SEA while maturing under Th1 or Th1/Th2 (T mix) promoting conditions. DCs exposed to SEA whilst maturing under Th2 promoting conditions, will upon co-culture with naГЇve T-cells induce a T-cell population that was less susceptible to HIV-1 R5 infection (p<0.05) compared to DCs unexposed to SEA, whereas HIV-1 X4 virus infection was unaffected. We determined that SEA, specifically through kappa-5, can potently bind to DC-SIGN and thereby blocks DC-SIGN mediated HIV-1 trans-infection (p<0.05) whilst not interfering with cis-infection. Here we analyzed the effects that soluble egg antigen (SEA) from Schistosoma mansoni had on modulating HIV-1 infection and cytokine/chemokine production in vitro. Such effects will likely have consequences for HIV-1 transmission and disease progression. Parasitic helminths evade, skew and dampen human immune responses through numerous mechanisms.

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