This question has been addressed by several investigators and the results of their studies have not been the same. In a study carried out in Ethiopia, we observed a highly significant correlation between helminth load (amount of eggs excreted in the stools) and HIV-1 plasma VL, in Ethiopians co-infected with helminths and HIV-1 (51). In a more recent study in Kenya (52), mother-to-child transmission of HIV-1 was found to be significantly associated with the presence of helminth infection in the mother and with immune reactivity of the mother's lymphocytes to the helminth infection, suggesting that indeed helminths impact on HIV-1 infection and probably on HIV-1 VL, though this was not reported in that article. However, in another study that we have carried out in Zambia (53), as well as in studies carried out in Kenya and Uganda (54,55), such associations were not observed. With regard to other co-infections, Wolday et al. observed increased HIV-1 VL in Leishmania HIV-1 co-infected individuals (51) and likewise, increased HIV-1 VL has been observed in malaria and TB dually infected patients (56–59). In a recent small but very convincing study on this issue in primates, Chenine et al. showed that rhesus macaques infected with Schistosoma mansoni, developed higher SHIV plasma levels in comparison with Schistosoma non-infected animals, following inoculation of the virus, and regardless of the intensity of the parasite infection (60). Furthermore, re-exposure of the SHIV-infected animals to Schistosoma, resulted in significant increase of SHIV viral load. Thus, this study demonstrated for the first time that primates co-infected with schistosomes, showed increased replication of immunodeficiency viruses, both in the acute and the chronic phases of the parasite infection, and that this was accompanied by a Th2 shift of the immune profile. With regard to the natural course of the HIV-1 infection, we suggested at the time, that helminth co-infection may contribute to an increase in HIV-1 VL in dually infected populations, and that therefore this could account for the faster progression of HIV-1 infection presumed to be present in Africa. By now, however, it is quite clear that the natural course of HIV-1 infection in Africa may be quite similar to that observed in the developed world, though poor medical, nutritional and other environmental factors may still be dominant in the outcome and contribute to increased mortality and morbidity in the HIV-1-infected population in Africa (61). Moreover, in studies carried by us on HIV(+) ETH in Israel, we have not seen any differences in the rate of progression between the ETH and the non-Ethiopian HIV(+) people living in Israel (24), though this study was carried out after eradication of worms in the Ethiopian immigrants.