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Acute Schistosoma mansoni Infection Increases Susceptibility to Systemic SHIV Clade C Infection in Rhesus Macaques after Mucosal Virus Exposure

26 Aug 2008

Marcia Triunfol

Source: PLoS Neglected Tropical Diseases (see original article)

Citation: Chenine A, Shai-Kobiler E, Steele LN, Ong H, Augostini P, et al. (2008). Acute Schistosoma mansoni Infection Increases Susceptibility to Systemic SHIV Clade C Infection in Rhesus Macaques after Mucosal Virus Exposure. PLoS Neglected Tropical Diseases 2(7): e265

The vast majority of individuals living with HIV-1/AIDS live in sub-Saharan Africa. This huge incidence of HIV-1/AIDS infection in the region corresponds approximately to 65% of all HIV-1/AIDS infected individuals. The region is also known for being endemic for many other pathogens, including Schistosoma mansoni, the agent that causes schistosomiasis.

Researchers are now investigating whether helmintic infections can exacerbate host susceptibility for a de novo viral infection, which could in part explain the disproportionately high incidence of HIV infection in sub-Saharan Africa. Previous studies have indicated that parasitic worm infections can indeed increase the chances of HIV infection, but these studies were limited, as they were either in vitro studies that evaluated the exposure of cells to the virus or they were epidemiological studies that tried to co-relate the use of anthelmintic medication with viral loads in individuals infected with both S. mansoni and HIV.

The study of Chenine and colleagues is the first to address this issue in a relevant animal model, namely the rhesus monkey. To do that, researchers worked with schistosome-infected and schistosome-free macaques that were exposed to low doses of the R5-tropic SHIV-C strain, which was inoculated intrarectally. The R5-tropic SHIV-C strain is responsible for almost 90% of all infections that occur by mucosal transmission, which was the main transmission route tested in this study.

The study reveals that infection by S. mansoni decreases the SHIV-C viral dose that is necessary to establish infection. While schistosome-free animals required a virus stock dilution of 1:50 to develop a de novo SHIV-C infection, schistosome-infected animals became infected with a mere 1:300 virus stock dilution. Additionally, the viral load found in those animals previously infected with the worm parasite was much higher than that observed in worm-free macaques. Therefore, besides infection susceptibility, the viral replication rate is also increased in co-infected animals. The study suggests that CD4+ T cells from co-infected animals are more permissive to viral infection and replication, which explains why co-infected animals have a much higher viral load, even though the viral inoculum used in schistosoma-infected animals was much lower (1:85) when compared with the one used in schistosoma-free animals (1:23).

As the authors point out, it may be possible that the increased susceptibility to HIV/AIDS that is observed in co-infected animals is limited to a viral infection that occurs exclusively through the rectal route, as this is the same route for the parasite egg excretion, which may compromise the integrity of the mucosa in the rectal area. Nevertheless, this study may lead to new HIV/AIDS-related public health policies that may now also consider the prevention, treatment and control of schistosomiasis as a way to decrease the spread of HIV/AIDS not only in Africa, but worldwide.

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Source

Title:
Acute Schistosoma mansoni Infection Increases Susceptibility to Systemic SHIV Clade C Infection in Rhesus Macaques after Mucosal Virus Exposure.

Authors:
Chenine AL, Shai-Kobiler E, Steele LN, Ong H, Augostini P, Song R, Lee SJ, Autissier P, Ruprecht RM, Secor WE

References:
PLoS Negl Trop Dis 2008: Vol. 2 no. 7, pp. e265

Abstract:
BACKGROUND: Individuals living in sub-Saharan Africa represent 10% of the world's population but almost 2/3 of all HIV-1/AIDS cases. The disproportionate HIV-1 infection rates in this region may be linked to helminthic parasite infections that affect many individuals in the developing world. However, the hypothesis that parasite infection increases an individual's susceptibility to HIV-1 has never been prospectively tested in a relevant in vivo model. METHODOLOGY/PRINCIPAL FINDINGS: We measured whether pre-existing infection of rhesus monkeys with a parasitic worm would facilitate systemic infection after mucosal AIDS virus exposure. Two groups of animals, one consisting of normal monkeys and the other harboring Schistosoma mansoni, were challenged intrarectally with decreasing doses of R5-tropic clade C simian-human immunodeficiency virus (SHIV-C). Systemic infection occurred in parasitized monkeys at viral doses that remained sub-infectious in normal hosts. In fact, the 50% animal infectious (AID(50)) SHIV-C dose was 17-fold lower in parasitized animals compared to controls (P<0.001). Coinfected animals also had significantly higher peak viral RNA loads than controls (P<0.001), as well as increased viral replication in CD4(+) central memory cells (P = 0.03). CONCLUSIONS/SIGNIFICANCE: Our data provide the first direct evidence that acute schistosomiasis significantly increases the risk of de novo AIDS virus acquisition, and the magnitude of the effect suggests that control of helminth infections may be a useful public health intervention to help decrease the spread of HIV-1.

PMID: 18648516
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