It is now widely accepted that by undermining the human immune response, HIV infections facilitate the establishment of opportunistic parasite infections such as Pneumocystis spp., microsporidia, and Cryptosporidium spp. [33–35]. Indeed, our findings show that the prevalence of Cryptosporidium spp. in the HIV-infected population was 10.1%, significantly higher than that of 3.1% among HIV-negative group. The immune profile of HIV-infected individuals was markedly different from that of their HIV-negative peers. However, no significant change in immune system indicators was observed when individuals with HIV infections but no parasite co-infection were compared to those with such co-infections. Cryptosporidium spp. infections in HIV-infected individuals often cause severe diarrhea and malnutrition, and can even lead to death among AIDS patients .
B. hominis is one of the most common human intestinal parasite infections. B. hominis is usually considered a commensal (non-pathogenic) protozoa inhabiting the human intestine, although previous studies have suggested that it has certain pathogenicity [37–39]. Interestingly, the prevalence of B. hominis among HIV-infected individuals was actually lower than that among the controls in our study.
The appropriate immune reaction against helminth infections is believed to be provided by Th2 cells which inhibit the development of Th1 cells, and hence prevent them and macrophages from mounting massive immune reactions against the comparatively very large parasites – a reaction which would potentially be harmful for the human body [40, 41]. The progression from HIV infection to AIDS is characterized by a decrease of Th1-type immune responses whereas Th2-type responses increase [42–44]. In our study, 6.3% of the HIV-infected participants were co-infected with intestinal helminthes, and the level of IFN-γ and IL-10 was lower among these co-infected individuals while the level of IL-4 was higher. The Th2-type immune response was elevated and the T value (T = Th1 / (Th1 + Th2) decreased. Thus, the co-infection of HIV and helminths acted synergistically in shifting the Th1/Th2 balance which might indicate an acceleration of the progress from HIV infection to AIDS. It was further observed that in individuals with HIV and B. hominis co-infection, CD4 levels were slightly lower compared to individuals without a B. hominis infection, while IFN-γ and other cytokine levels did not change significantly and IL-2 levels were higher. IL-2 is indispensable for cell-mediated immune responses against parasitic infections and humoral immunity. Therefore, the presence of B. hominis may even be favorable for HIV-positive individuals as IL-2 induces T cells to secrete IFN-γ, and the latter is an important factor in anti-viral immune reactions. The promotion of human B cell proliferation should inhibit IL-4. However, in our study IL-4 levels were found to be slightly higher. To sufficiently determine the reasons, further studies need to be conducted. The IL-10 level was slightly lower if co-infection of HIV and B. hominis was present. IL-10 can inhibit Th1-stimulating cytokine secretion. Together, these findings indicate, once again, a need to further study the pathogenicity of B. hominis in order to better determine its status as a member of the intestinal flora [45–47].
In conclusion, co-infection with helminths was associated with potentially detrimental changes of the immunologic profile of HIV-infected individuals. Helminth infections appeared to act synergistically with HIV in shifting the Th1/Th2 balance, a shift which has traditionally be seen as indicative of an acceleration of the progress from HIV infection to AIDS. On the other hand, co-infection with protozoa was imperceptible in the immune response profile: co-infection with Cryptosporidium spp. was not associated with any significant change in studied immune factors while co-infection with B. hominis was associated with favorable shifts in the immune profile.