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HIV and immune reconstitution disease in the wormy world

Nacher, Mathieua,b; Carme, Bernardb,c; Couppié, Pierreb,d

doi: 10.1097/QAD.0b013e3282efb8e9

aCOREVIH Cayenne General Hospital, Cayenne, French Guiana

bEquipe EA 3593, Université Antilles Guyane, Campus Saint Denis, Cayenne, French Guiana

cDepartment of Parasitology-Mycology, Cayenne General Hospital, Cayenne, French Guiana

dDepartment of Dermatology, Cayenne General hospital, Cayenne, French Guiana.

Received 22 June, 2007

Accepted 4 July, 2007

In tropical countries, notably sub-Saharan Africa, helminth infections are the most prevalent parasitic infection. These great immunomodulators have the ability to tip the balance towards T-helper cell type 2 immunity, to decrease vaccine responses, and influence the outcome of major tropical killers. For example, intestinal helminths seem to play a protective role against severe malaria by blunting proinflammatory cytokines [1]. On the contrary, there is a negative impact of helminths on the immunity and clinical course of tuberculosis [2]. Several conflicting studies have been published comparing viral loads and CD4 cell counts in HIV-infected individuals with and without helminths. It is currently not known whether helminths have any significant impact on the course of HIV infection. With the scaling up of antiretroviral use in poor countries, a growing number of individuals are undergoing treatment in areas of a high prevalence of helminth infection. When available, HAART is usually started at lower CD4 cell counts than in rich countries, where routine CD4 cell counts usually allow clinicians to start treatment before opportunistic infections occur. Given the poor diagnostic facilities of most health structures in the developing world, a number of patients start HAART while having a latent opportunistic infection. The combination of a very low CD4 cell count and undiagnosed infection at the start of HAART are ideal conditions for immune reconstitution disease (IRD) to occur. This can partly explain the very high mortality rate during the first year of HAART observed in numerous trials conducted in Africa. The incidence and mortality of IRD vary widely between publications. This is attributed to differences in the severity of immunodeficiency, the prevalence and intensity of co-infections when HAART is initiated, and maybe genetic factors [3]. We suggest the wide variation between estimates of the incidence and mortality of IRD could mirror the variation in the prevalence of helminth infections between different study sites. The postulated immune mechanism of IRD involves an imbalance between proinflammatory (IFN-γ) and homeostatic cytokines (IL-10), a mechanism that is significantly affected by helminth infections. Therefore, a simple prediction that would arise from the immunological impact of helminths is that helminth-infected HIV patients starting HAART would have less severe IRD than patients without helminths infected with the same pathogen at equivalent disseminations. Such knowledge may lead to important recommendations regarding the management of helminth infections during HAART initiation.

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© 2008 Lippincott Williams & Wilkins, Inc.