Associations between helminth infection and CD4+ T cell count, viral load and cytokine responses in HIV-1-infected Ugandan adults

Abstract

It has been proposed that helminth infection may exacerbate HIV progression by promoting activation of 'type 2' immune responses. To examine this hypothesis, we investigated helminth infection in a cohort of HIV-1-seropositive adults in Entebbe, Uganda, during November 1999 to January 2000. Individuals with helminths were treated. At enroLlment, after 5 weeks and after 4 months, CD4+ and CD8+ T cell counts and viral load were measured. Cytokine responses (interferon [IFN]-gamma, interleukin [IL]-2, IL-4 and IL-5) to Schistosoma mansoni adult worm antigen (SWA), Mycobacterium tuberculosis culture filtrate proteins (CFPs) and phytohaemagglutinin (PHA) were measured in a whole blood assay. At baseline, CD4+ T cell counts and CD4+: CD8+ ratios were higher in individuals with helminths than in those without (median CD4+ T cell counts 467/microL and 268/microL, respectively, P = 0.005). Viral load was lower among those with helminths but this was not statistically significant. During follow-up, CD4+ T cell counts and cytokine responses to PHA fell among individuals without helminths. Among those treated for helminths, CD4+ counts remained stable. Viral loads showed a transient increase at 5 weeks, which was more marked among those treated for helminths, but the levels at 4 months were similar to baseline in both groups. Among those with schistosomiasis, IFN-gamma and IL-2 responses to CFP, and IL-2 and IL-4 responses to PHA declined but there was a sustained increase in cytokine responses to SWA following treatment. These data do not support the hypothesis that helminth infection exacerbates HIV infection. The possibility that chronic helminth infection may suppress HIV replication and that effects on HIV replication may vary during helminth infection and treatment should be considered.

Association of Schistosomiasis and HIV Infection in Tanzania

“…34 S. mansoni infection was also shown to increase the HIV RNA viral load in HIV-positive patients with untreated S. mansoni infection compared with patients with S. mansoni infections that had been treated. 35 Several earlier non-randomized studies did not find an effect of praziquantel treatment on viral load, 5,6,36,37 but this result has been postulated to be caused by transient increases in the schistosomiasis-conducive Th2 environment immediately after treatment.…”

“…Rhesus macaques with active S. mansoni infection were 17 times more susceptible to simian HIV (SHIV) acquisition after rectal inoculation than macaques without S. mansoni. 4 Although a variety of interactions between S. mansoni and HIV infection in humans have been described, [5][6][7][8][9][10] a direct association between active S. mansoni and HIV has not been documented in humans. If S. mansoni is a risk factor for HIV acquisition, this finding could have major implications for HIV prevention work in much of the world.…”

Intestinal parasitic infections in HIV/AIDS patients: epidemiological, nutritional and immunological aspects

“…Few studies have reported the relationship between cytokines in individuals with HIV and parasitic intestinal infections. Some authors evaluated cytokines and their relationship with parasites such as Schistosoma mansoni, Wuchereria bancrofti, and Trichinella spiralis (71)(72)(73)(74)(75)(76)(77)(78)(79). No correlation between serum INF-γ, IL-2, and IL-10 levels and intestinal parasitic infections was seen.…”

Practical Management of HIV-Associated Anemia in Resource-Limited Settings: Prospective Observational Evaluation of a New Mozambican Guideline

“…[2][3][4] Malaria incidence and severity are greater in the presence of HIV, and the prognosis of HIV infection may be altered by concurrent helminth infection and/or deworming. [5][6][7][8] Opportunistic and other complications of HIV infection further increase anemia risk. HIV viremia impairs hematopoiesis.…”