Nega Berhe

Treatment of intestinal worms is associated with decreased HIV plasma viral load

Background: 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. Objective: To study the effect of antihelminthic treatment on HIV plasma viral load (VL) in HIV‐ and helminth‐infected individuals living in Ethiopia. Methods: 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. Results: 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) Conclusions: 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.

Hiv viral load and response to antileishmanial chemotherapy in co-infected patients

OBJECTIVEnTo investigate whether clearance of Leishmania parasites from tissue aspirate smears in patients with HIV and visceral leishmaniasis (VL) co-infection treated with pentavalent antimonials is influenced by initial HIV viral load and to assess the effect of active VL on HIV viral load and replication in vivo.nnnMETHODSnLeishmania parasites were identified in Giemsa-stained smears prepared from tissue aspirates. Parasite index was determined by quantifying Leishmania donovani bodies in smears. HIV-1 RNA was quantitated by using the nucleic acid sequence-based amplification technique with a limit of detection of 500 copies/ml. All patients were treated with pentavalent antimonials at 20 mg pentavalent antimony (Sb(V))/kg daily for a total of 28 days. None of the patients received specific anti-retroviral therapy.nnnRESULTSnSeventeen patients (73.9%) showed good initial response to anti-leishmanial treatment and the remaining six (26.1%) had very poor response. Among the good responders, 11 (64.7%) had no demonstrable Leishmania donovani bodies in post-therapy tissue aspirate smear preparations, and in the remaining six (35.3%) their parasite loads were reduced to very low levels. Patients with poor response had persistently high parasite index despite completion of anti-leishmanial chemotherapy. Poor responders had pre-treatment median HIV viral load that was >160-fold higher than responders to anti-leishmanial chemotherapy; [410000 copies/ml (quartile range, 33000-530000) and 2500 copies/ml (quartile range 500-297500), respectively]. Furthermore, compared with pre-treatment viral concentrations, patients with good response showed marked reduction in post-treatment viral load. In contrast, post-treatment HIV viral concentrations were markedly increased among patients with poor response to anti-leishmanial therapy.nnnCONCLUSIONSnThe results suggest that pre-treatment HIV viral load influences response to anti-leishmanial chemotherapy and active VL is associated with increased viral replication in vivo, supporting the notion that dual infection plays an important role in the pathogenesis and disease progression of either infection.

HIV-1 alters T helper cytokines, interleukin-12 and interleukin-18 responses to the protozoan parasite Leishmania donovani.

ObjectiveTo investigate the in vitro and in vivo effect of HIV-1 on lymphoproliferative and T helper (Th) cytokine responses in leishmaniasis. MethodsTh1 [interleukin (IL)-2 and interferon (IFN)-γ] and Th2 (IL-4 and IL-10) as well as IFN-γ-inducing cytokines (IL-12 and IL-18) were measured in antigen and mitogen-stimulated culture supernatants of peripheral blood mononuclear cells (PBMC) of healthy donors, HIV-infected and visceral leishmaniasis (VL) patients with or without HIV co-infection. ResultsProliferative responses to phytohaemagglutinin (PHA) were significantly lower in PBMC from VL and asymptomatic HIV-infected persons compared with responses in healthy individuals. VL–HIV co-infected patients showed the lowest responses. Although there was no significant difference in the Leishmania-induced proliferative responses among the healthy group and those infected with HIV only, VL patients (with or without HIV) exhibited very low proliferation. When cultured with PHA or Leishmania, PBMC from healthy donors produced high levels of a Th1 cytokine (IFN-γ) and low levels of Th2 cytokines (IL-4 and IL-10). In addition, co-culturing PBMC from healthy donors with a killed HIV preparation abrogated the production of IFN-γ induced by Leishmania and augmented IL-4 and IL-10 production. Cells from HIV-infected patients produced low levels of IFN-γ, but high levels of IL-10. The addition of anti-IL-10 did not increase Leishmania-induced proliferative responses or IFN-γ production. Both IL-12 and/or IL-18 responses were lower in VL patients, HIV-infected, or VL–HIV co-infected patients as compared with those of healthy donors. ConclusionThe data suggest that the inhibitory effect of HIV and VL on proliferation and IFN-γ production is not due to IL-10 alone, but that the defect induced by HIV and VL probably operates at the level of regulation of IFN-γ-inducing factors, such as IL-12 and IL-18.

Association of Total Levels of Serum Antioxidants with Periportal Fibrosis andIntensity of Schistosoma mansoni Infections in Cheretee, North East Ethiopia

Schistosomiasis is only second to malaria in terms of public health importance among parasitic diseases. Hence morbidity and mortality associated with Schistosoma mansoni are mainly the result of periportal fibrosis of the liver. With the objective of evaluating the association of total serum antioxidants and intensity of S. mansoni infection a cross sectional study was conducted from February 2011 to June 2011 involving 414 individuals and 30 controls from S. mansoni non-endemic area. The study groups were selected using systematic random sampling technique and data were collected using a pre-tested clinical questionnaire, ulthersonographic examinations of the liver and serum ferric reducing antioxidant power (FRAP) assays. Prevalence of Schistosoma mansoni infection and periportal fibrosis in Cheretee was 36.72% and 9.42%, respectively. Prevalence of periportal fibrosis and intensity of infection had a sharp rise in the age group 11-20 years, reached its peak in the 21 to 30-year age group, and started to decline thereafter up to >40. Age, sex and intensity of infection were strongly associated with periportal fibrosis development (p<0.05). Mean total serum antioxidant concentrations were significantly lower in study subjects who were from S. mansoni endemic area (96.5 μM/L) compared with healthy participants from Addis Ababa (339.9 μM/L). However, mean total serum antioxidant concentration were not significantly different among PPF positive and negative individuals from S. mansoni endemic area. Finally, further studies are recommended on the cause of this low antioxidant concentration.