We have previously suggested that helminthic infections make the host more susceptible to HIV infection and enhance its progression due to the chronic immune activation they cause.
To study the effect of antihelminthic treatment on HIV plasma viral load (VL) in HIV- and helminth-infected individuals living in Ethiopia.
Fifty-six clinically asymptomatic HIV-1-infected individuals, 31 (55%) of whom were also infected with helminths, were studied. All participants received antihelminthic treatment at baseline and at 3 and 6 months. Worm egg excretion, HIV plasma VL, and T-cell subsets were determined at baseline and 6 months after treatment.
The mean age, number of CD4 T cells, and gender distribution were similar in the helminth-infected and -noninfected groups. At baseline, HIV plasma VL was strongly correlated to the number of eggs excreted (p < .001) and was higher in individuals infected with more than one helminth (5.28 ± 0.35 versus 4.30 ± 1.13 log10 RNA copies/mL, respectively; p = .16). After treatment of helminths, the 6-month change in HIV plasma VL was significantly different between the successfully treated group and the persistently helminth-positive group (p = .04)
Helminth "load" is correlated to HIV plasma VL, and successful deworming is associated with a significant decrease in HIV plasma VL. The results of the current study, if confirmed in a larger study, may have important implications for slowing disease progression and reducing risks of transmission.
*Armauer Hansen Research Institute, Addis Ababa, Ethiopia; †Hebrew University Hadassah Medical School, AIDS Clinic, Department of Clinical Microbiology and Infectious Diseases, Hadassah Hospital, Jerusalem, Israel; ‡Department of Gynaecology and Obstetrics, and ||Infectious Diseases Unit, Department of Internal Medicine, Black-Lion Teaching Hospital, Addis Ababa, Ethiopia; §Institute of Pathobiology, Addis Ababa University, Addis Ababa, Ethiopia; ¶Unit for Infectious Disease, Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden; #Ben-Gurion University, Department of Epidemiology, Beer Sheba, Israel; **Department of Immunology and Microbiology, Rush Medical School, Chicago, IL, U.S.A.; and ††Ruth Ben-Ari Institute of Clinical Immunology and AIDS Center, Hebrew University Hadassah Medical School, Kaplan Medical Center, Rehovot, Israel
This study was supported in part by grants from the Institute of Advanced Therapy for the Center of Excellence in AIDS Research, Israel; the Horowitz Foundation, Israel; the AIDS Center of Hadassah Hospital, Israel; and the Rush Medical School, Chicago, IL, U.S.A.
Address correspondence and reprint requests to Zvi Bentwich, Rosetta Genomics, 18 Halsela Street, Ein Karem, Jerusalem 95742, Israel; e-mail: zbentwich@rosettagenomics.com
Manuscript received January 17, 2002; accepted May 28, 2002.