Helminth Infections and HIV: A Double Hit

Jill E. Weatherhead, MD; Laila Woc-Colburn, MD

Disclosures

October 21, 2014

Parasitic Diseases and Treatment Effects in HIV Coinfection

Initiation of treatment and mass drug administration against helminths in areas of heavy worm burden may have an impact on HIV rates. A decrease in parasitic load after worm elimination promotes immune system reconstitution and might reduce HIV viral load, increase CD4 counts, and delay time to development of AIDS by as much as 3.5 years.[1,2,7,13]

A randomized, double-blinded, placebo-controlled trial conducted in Kenya showed significantly higher CD4 counts and a trend toward lower plasma HIV-1 viral loads after albendazole treatment of individuals with documented Ascariasis lumbricoides infection.[14,15] Despite this positive outcome, studies with larger numbers of patients who harbor other types of helminth infections have been unable to replicate these findings.[7]

Routine empirical deworming of patients with HIV in endemic helminth regions has not been shown to delay HIV disease progression (as defined by CD4 count or HIV RNA levels) in adults who are ineligible for HAART.[14] Differences in study findings suggest that the variability in geographical distribution of individual helminth species, as well as species-specific host responses, both influence the relative benefit of deworming in coinfected individuals.[7,13,14]

Treatment of such parasitic infections as ascariasis, schistosomiasis, and lymphatic filariasis might delay HIV-1 disease progression, whereas treatment of other parasites, such as Trichuris and hookworm species, might not.[1] This difference in response could be a consequence of tissue invasiveness, antigen burden, duration of infection, or degree of host immune response.[1] Ascariasis may induce a more pronounced Th2 polarization such that coinfected patients who receive therapy have larger swings in immune function, promoting improved HIV-1 control after deworming.[3]

Because of these discrepancies, empirical episodic deworming efforts have targeted such high-risk groups as women of childbearing age, adults in high-risk occupations, and preschool and school-aged children who are at high risk for reinfection.[14] Overall, the effects of anthelmintic treatment on HIV viral load and CD4 reconstitution have been variable, and further studies are required to evaluate species-specific clinical outcomes after deworming in coinfected HIV patients.[2,4]

Effect on Vaccines

Vaccine development is integral to the control and prevention of HIV and helminth infections in highly prevalent areas worldwide. It is possible that a vaccine against HIV-1 will be able to protect a large helminth-coinfected population.[4] However, the effects of geohelminths on vaccine-induced immune mucosal response remains an area of uncertainty.[4] This interaction has been shown with other oral mucosa vaccines, in which albendazole treatment of ascariasis enhanced the response to oral cholera vaccine in children[4] and S mansoni-infected mice had enhanced interferon gamma response to an HIV-1 clade C DNA vaccine after praziquantel treatment.[4] Furthermore, helminth vaccination may be impeded in people with poorly controlled HIV infection, depending on the type of vaccine.

Studies have shown that vaccinations in children with HIV tend to be less immunogenic than in children without HIV and protective antibody titers, and they have rapid waning of vaccine-induce immunity.[11] It is evident that helminth and HIV coinfections have intricate interactions that require further study to enable us to protect an at-risk population from progression of disease, and to facilitate eradication of pathogens.

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