Immune activation and induction of HIV-1 replication within CD14 macrophages during acute Plasmodium falciparum malaria coinfection

Pisell, Tracy L.; Hoffman, Irving; Jere, Charles S.; Ballard, Sarah-Blythe; Molyneux, Malcolm E.; Butera, Salvatore T.; Lawn, Stephen D.

doi:10.1097/00002030-200207260-00007

Cited by 45 publications

(37 citation statements)

References 34 publications

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“…45 Another mechanism involves glycosylphosphatidylinositol (GPI), the anchorage of covalently linked merozoite antigens such as MSP-1 and MSP-2, which can also induce TNF-a production and secretion by macrophages. 49 An effect of the GPI toxin on vascular endothelial cells is the upregulation of various host receptors involved in tissue-specific IRBC sequestration such as intercellular adhesion molecule-1 (ICAM-1) in human umbilical cord veins 40,50 and in trophoblast cells. 51 ICAM-1 is also involved in monocyte adhesion and promotes accumulation in trophoblastic intervillous spaces 52 that could facilitate HIV mother-to-child transmission.…”

Section: Biological Mechanisms Of Hiv and Malaria Interaction In Pregmentioning

confidence: 99%

Placental malaria, maternal HIV infection and infant morbidity

Briand

Badaut

Cot

2009

Annals of Tropical Paediatrics

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Co-infection with malaria and HIV in pregnant women is particularly common in sub-Saharan Africa and has serious consequences for both mother and newborn child. Numerous studies have been published on the effects in pregnancy of HIV on malaria infection and on the effects of malaria on HIV infection. The increased prevalence and intensity of parasitaemia (placental and peripheral infection and parasite density) in HIV-infected women is well established. Similarly, malaria infection seems to be associated with higher viral loads. However, there is still uncertainty as to the influence of malaria on the clinical course of HIV infection, mother-to-child transmission of HIV, and the consequences of co-infection on post-neonatal infant morbidity and mortality. These questions require further investigation. In terms of prevention, intermittent preventive treatment with two doses of sulfadoxine-pyrimethamine (SP) has been found less effective in preventing malaria in HIV-infected than uninfected women, and a higher dosage (such as monthly SP) has been recommended. Regarding malaria, there is also a lack of clear recommendations for women taking daily cotrimoxazole prophylaxis, and anti-malarial-anti-retroviral interactions are not well understood. Multi-centre clinical trials should be undertaken to investigate effective, coherent and well-tolerated strategies to prevent malaria in HIV-infected women. Safe alternatives to SP should be identified and evaluated rapidly. Finally, a central pharmaco-vigilance network should be instituted to report adverse effects.

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Section: Biological Mechanisms Of Hiv and Malaria Interaction In Pregmentioning

confidence: 99%

Placental malaria, maternal HIV infection and infant morbidity

Briand

Badaut

Cot

2009

Annals of Tropical Paediatrics

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“…The infection has been demonstrated to induce expression of inflammatory and pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-␣), interferon-alpha (IFN-␣), interferon-gamma (IFN-␥), and interleukin-6 (IL-6), which result in inhibition of parasite growth. Moreover, malaria has also been shown to significantly stimulate HIV-1 replication (Xiao et al, 1998;Chougnet et al, 2001;Freitag et al, 2001;Kublin et al, 2005;Pisell et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Prevalence of malaria and HIV coinfection and influence of HIV infection on malaria disease severity in population residing in malaria endemic area along the Thai–Myanmar border

et al. 2015

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“…This cell type not only appears to use alternate assembly and budding pathways but also is an important cell lineage for HIV-1 transmission, establishment and maintenance of infection, and pathogenesis (36,37,57).…”

mentioning

confidence: 99%

Proteomic and Biochemical Analysis of Purified Human Immunodeficiency Virus Type 1 Produced from Infected Monocyte-Derived Macrophages

Chertova

Chertov

Coren

et al. 2006

J Virol

408

470

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Human immunodeficiency virus type 1 (HIV-1) infects CD4؉ T lymphocytes and monocytes/macrophages, incorporating host proteins in the process of assembly and budding. Analysis of the host cell proteins incorporated into virions can provide insights into viral biology. We characterized proteins in highly purified HIV-1 virions produced from human monocyte-derived macrophages (MDM), within which virus buds predominantly into intracytoplasmic vesicles, in contrast to the plasmalemmal budding of HIV-1 typically seen with infected T cells. Liquid chromatography-linked tandem mass spectrometry of highly purified virions identified many cellular proteins, including 33 previously described proteins in HIV-1 preparations from other cell types. Proteins involved in many different cellular structures and functions were present, including those from the cytoskeleton, adhesion, signaling, intracellular trafficking, chaperone, metabolic, ubiquitin/proteasomal, and immune response systems. We also identified annexins, annexin-binding proteins, Rab proteins, and other proteins involved in membrane organization, vesicular trafficking, and late endosomal function, as well as apolipoprotein E, which participates in cholesterol transport, immunoregulation, and modulation of cell growth and differentiation. Several tetraspanins, markers of the late endosomal compartment, were also identified. MDM-derived HIV contained 26 of 37 proteins previously found in exosomes, consistent with the idea that HIV uses the late endosome/multivesicular body pathway during virion budding from macrophages.As an RNA virus with limited coding capacity, human immunodeficiency virus type 1 (HIV-1) subverts cellular pathways and processes to facilitate many aspects of its replication cycle. It is known that a variety of cellular factors are involved in HIV-1 assembly and budding (13,20,42,44). Typically, HIV-1 is observed by electron microscopy to assemble at and bud from the plasma membrane in T cells and the epithelial cell lines that serve as models for HIV-1 assembly studies (23). In contrast, in macrophages, one of the primary target cell populations in vivo, HIV-1 appears to assemble mostly at internal late endosomal and multivesicular body (MVB) membranes and then bud into these vesicular structures, observable in electron micrographs as internal virion-filled compartments (48,54,55,59). After budding into MVB, these virion-laden vesicles are presumably transported to the cell surface and virus is released from the cell by a normal exocytotic fusion of these structures with the plasma membrane, thereby releasing the contents of the MVB (54, 55).To date, the differences in viral and cellular protein interactions involved in assembly and budding at the plasma membrane versus the late endosomal assembly pathway remain unclear. Clues to the location and the mechanism by which HIV-1 buds can be provided by the cellular proteins that are incorporated into virions. In the case of macrophage-derived virus, the presence of HLA class II and other late endosoma...

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Immune activation and induction of HIV-1 replication within CD14 macrophages during acute Plasmodium falciparum malaria coinfection

Abstract: Acute P. falciparum malaria coinfection impacts virus-host dynamics in HIV-1-infected persons at the cellular level, notably showing a reversible induction of HIV-1 replication in CD14 macrophages that is associated with changes in immune activation.

Cited by 45 publications

References 34 publications

Placental malaria, maternal HIV infection and infant morbidity

Placental malaria, maternal HIV infection and infant morbidity

Prevalence of malaria and HIV coinfection and influence of HIV infection on malaria disease severity in population residing in malaria endemic area along the Thai–Myanmar border

Proteomic and Biochemical Analysis of Purified Human Immunodeficiency Virus Type 1 Produced from Infected Monocyte-Derived Macrophages

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