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Archived Comments for: Effect of malaria on HIV/AIDS transmission and progression

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  1. Effect of parasites on HIV/AIDS transmission and diseases progression: Consideration of HIV-1 viral factors

    Andargachew Mulu, Institute of Virology, University of Leipzig, Germany and Department of Microbiology, University of Gondar, Ethiopia

    21 September 2013

    The review by Alemu et al (1) summarized recent evidences on the negative impact of malaria infection on HIV. It also provides certain immunological mechanism how malaria increases HIV-RNA viramea and which further facilitate HIV diseases progression (1). I personally found it very suitable although it lacks to include the evolutionary dynamics of HIV during malaria infection. I believe the authors will come up a second review characterizing the impact of malaria immunological correlates on HIV viral genome.

    As a matter of chance in those areas with high malaria infection, there is also high rate of HIV infection and disease transmission. Moreover there are also high rates of helminths infection which are known to result immune activation linked with increase HIV RNA level and disease progression. Helminths, malaria and HIV-1 use multiple mechanisms to avoid immune responses. These mechanisms might interact each other and results important and/or deleterious consequences for the epidemiology and pathogenesis of each particular infection in various geo-ecological conditions. Considering the extent of geographical and epidemiological overlap of malaria (acute infection) and helminths (known to be chronic infections in the tropical settings of Africa) with HIV, there have been limited and inconsistent evidence of important interactive effects. Similarly, strong evidence for a beneficial effect of anti-malarial and anti-helminthic treatment of malaria and helminth-HIV-1 co-infected individuals on viral load and/or CD4 cell counts are lacking. Most studies do not consider viral factors and their interaction with parasitic and host factors during HIV-malaria-helminths co-infections. Recently we have observed significantly higher HIV RNA level among helminths-HIV infected individual compared with helminths non infected HIV infected controls which was interestingly declined 12 weeks after deworming (2). It is not apparent however that co-infection with HIV-1 and malaria and/or helminths will always be more detrimental to the host than either single infection alone, or that intervening against co-infections will have only beneficial effects.

    Certainly, the interaction of viral and host factors also influence the risk of HIV disease progression and plasma HIV RNA level (3). For example, the HIV-1 long-terminal repeat (LTR) located at both ends of the viral genome regulates viral gene expression by interacting with multiple viral and host factors. During acute and/or chronic HIV-1 infection with malaria and/or helminthic co-infection, the ensuing cytokine imbalances could conceivably lead to increased expression of co-receptor and transcriptional factors resulting in higher HIV RNA level and faster disease progression which may in turn result in active up-regulation of HIV LTR. Intracellular parasitic infection like leishmania was found to be a potential activator for HIV replication and potent inducer of LTR transcription and viral replication in vitro (4). Activation of HIV-1 LTR transcription in host cells through complex biochemical pathways involving the participation of transcriptional factor NF-¿B has been observed during leishmania parasite co-infection in vitro. Triple NF-¿B sequences have been described in most HIV-1C isolates (5, 6, Mulu et al. 2013-under review) and believed to influence the viral fitness and higher replication and transmission. However, the relationship between the occurrences of triple NF-¿B in most HIV-1C isolates and malaria and/or helminths co-infection is not known. Interestingly, we found triple NF-¿B sites and high sequence similarities among helminths infected and non infected HIV-1 subtype C Ethiopia patients (Mulu et al. 2012-under review). Nevertheless malaria parasites being intracellular could potentially influence the genetic variability of HIV-1C on some motives. Thus, reviewing available reports on the molecular mechanisms by which malaria and helminths co-infection increase HIV viraemia from both parasite, viral and host perspectives and by which their treatment reduce it and delays HIV-1 disease progression may lead to a better understanding of HIV-1 pathogenesis during malaria and/or helminths co-infection and shows possible future direction in the discipline.

    1. Alemu A, Shiferaw Y, Addis Z, Mathewos B, Birhan W: Effect of malaria on HIV/AIDS transmission and progression. Parasites and Vectors 2013, 6:18
    2. Mulu A, Maier M, Liebert UG: Deworming of intestinal helminths reduces HIV-1 subtype C viremia in chronically co-infected individuals. Int J Infect Dis 2013; doi:pii: S1201-9712 (13) 00157-4. 10.1016/j.ijid.2013.03.022
    3. Graziosi C, Soudeyns H, Rizzardi PG: Immunopathogenesis of HIV infection. AIDS Res Hum Retroviruses 1998, 14:S135-S142
    4. Olivier M, Badaro, Medrano FJ, Moreno J (2003) The pathogenesis of Leishmania/HIV co-infection: cellular and immunological mechanisms. Ann Trop Med Parasitol, 97, Suppl1: S79¿S98.
    5. Jeeninga E, Hoogenkamp M, Armand-Ugon M, et al: Functional Differences between the Long Terminal Repeat Transcriptional Promoters of Human Immunodeficiency Virus Type 1 Subtypes A through G. J Virol 2000, 74: 3740¿3751.
    6. Bachu M, Yalla S, Asokan M, et al: Multiple NF-¿B sites in HIV-1 subtype C LTR confer superior magnitude of transcription and thereby the enhanced viral predominance. J Biochem 2012,(

    Competing interests