Helminth Infections and HIV: A Double Hit

Helminth Infection and HIV

Helminth infections are common in tropical and subtropical areas of the globe. Worldwide, more than 2 billion people are infected with at least one helminth species.^[1] These areas of heavy helminth burden have significant geographic overlap with a high prevalence of HIV-1 infection. More than 22.5 million people in sub-Saharan Africa alone are estimated to be coinfected with HIV and helminths.^[2]

The interaction between chronic helminth and HIV-1 coinfection has become a focus of study, because both have profound effects on the host immune system. Helminth infection typically prompts a dominant type 2 T-helper–cell systemic immune system response, with induction of regulatory T cells; activation of immunosuppressive cytokines, including interleukin (IL)-4, IL-5, and IL-10; increased production of immunoglobulin IgE; and degranulation of mast cells.^[3,4,5]

On the other hand, HIV-1 is controlled by natural killer cells, CD8 T cells, and antibodies and destroys the host immune system through direct infection of CD4 T cells.^[5] Eventually, progressive destruction of CD4 T cells leads to immunodeficiency through CD4 T-cell depletion and down-regulation of type 1 helper T cells that modulate the progression to AIDS.^[4,5] The profound loss of Th1 immune cells in advanced AIDS is balanced with minimal reduction of Th2-mediated cytokine activity.^[5] This immunologic shift from Th1 to Th2 cytokine response in patients with HIV may serve as a marker of HIV progression.^[5]

Because both HIV and chronic helminth infections significantly alter the host immune system, shifting the balance between Th1 and Th2 activation, coinfection with HIV and different helminth species can influence the likelihood of pathogen establishment, growth, replication, and clearance; disease severity; and transmission.^[6] Theories on interactions between chronic helminth infections and HIV infection exist; however, the data remain inconclusive.

Studies have shown that coinfection with helminths in patients with HIV infection can increase cellular susceptibility to HIV-1 infection, which heightens susceptibility to HIV transmission, and down-regulating control of HIV-1 replication, which can augment viral replication and accelerate disease progression.^[2,3,6,7] Furthermore, studies have also shown an association between helminth infection and increased risk for mother-to-child transmission of HIV.^[4,7] Conversely, CD4 T-cell destruction from HIV-1 infection could also be a risk factor for increased susceptibility to or reduced clearance of helminth infection.^[4]

Certain antihelminth treatment regimens have been shown to be less effective in clearing helminth infections in HIV-1 infected persons with low CD4 counts. Compared with patients who do not have HIV infection, reinfection has also been shown to be more common after antihelminth treatment in HIV-infected persons with low CD4 counts.^[4] Significant reductions in the prevalence of ascariasis, trichuris, hookworm infection, and strongyloidiasis have also been reported after starting highly active antiretroviral therapy (HAART), suggesting that HAART improves immunologic protection and control of helminth infection.^[1]

Despite these associations, the overall relationship between helminths and HIV remains unclear and might vary with helminth burden and the specific helminth pathogen.^[6] Having a better understanding of the interactions between helminths and HIV could influence HIV-1 acquisition, disease progression, interaction with helminth vaccination, and eradication of helminth infection.^[4]

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