Mechanisms of interaction between protozoan parasites and HIV

Andreani, Guadalupe; Lodge, Robert; Richard, Dave; Tremblay, Michel J.

doi:10.1097/coh.0b013e32835211e9

Cited by 32 publications

(21 citation statements)

References 68 publications

(40 reference statements)

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“…In addition to acute coinfections, chronic infections, such as helminths or mycobacteria, significantly impact the immune responses to other infections or vaccines (reviewed in [52]). In leishmaniasis, HIV coinfection contributes to enhanced disease, as does simultaneous infection with schistosomes [53], [54]. Taken together these studies argue that fully understanding the outcome of one infection may require knowledge about additional ongoing infections.…”

Section: Discussionmentioning

confidence: 99%

Engagement of NKG2D on Bystander Memory CD8 T Cells Promotes Increased Immunopathology following Leishmania major Infection

et al. 2014

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One of the hallmarks of adaptive immunity is the development of a long-term pathogen specific memory response. While persistent memory T cells certainly impact the immune response during a secondary challenge, their role in unrelated infections is less clear. To address this issue, we utilized lymphocytic choriomeningitis virus (LCMV) and Listeria monocytogenes immune mice to investigate whether bystander memory T cells influence Leishmania major infection. Despite similar parasite burdens, LCMV and Listeria immune mice exhibited a significant increase in leishmanial lesion size compared to mice infected with L. major alone. This increased lesion size was due to a severe inflammatory response, consisting not only of monocytes and neutrophils, but also significantly more CD8 T cells. Many of the CD8 T cells were LCMV specific and expressed gzmB and NKG2D, but unexpectedly expressed very little IFN-γ. Moreover, if CD8 T cells were depleted in LCMV immune mice prior to challenge with L. major, the increase in lesion size was lost. Strikingly, treating with NKG2D blocking antibodies abrogated the increased immunopathology observed in LCMV immune mice, showing that NKG2D engagement on LCMV specific memory CD8 T cells was required for the observed phenotype. These results indicate that bystander memory CD8 T cells can participate in an unrelated immune response and induce immunopathology through an NKG2D dependent mechanism without providing increased protection.

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Section: Discussionmentioning

confidence: 99%

Engagement of NKG2D on Bystander Memory CD8 T Cells Promotes Increased Immunopathology following Leishmania major Infection

et al. 2014

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“…Infection with Plasmodium falciparum increases HIV-1 viral load and enhances progression to AIDS [284]. The enhancing effect of malaria on DC-mediated trans infection could be due to hemozoin, a pigment that is released in excess after destruction of the infected erythrocytes.…”

Section: Coinfections and Dc-mediated Hiv-1 Trans Infectionmentioning

confidence: 99%

HIV-1TransInfection of CD4⁺T Cells by Professional Antigen Presenting Cells

Rinaldo

2013

Scientifica

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Since the 1990s we have known of the fascinating ability of a complex set of professional antigen presenting cells (APCs; dendritic cells, monocytes/macrophages, and B lymphocytes) to mediate HIV-1 trans infection of CD4+ T cells. This results in a burst of virus replication in the T cells that is much greater than that resulting from direct, cis infection of either APC or T cells, or trans infection between T cells. Such APC-to-T cell trans infection first involves a complex set of virus subtype, attachment, entry, and replication patterns that have many similarities among APC, as well as distinct differences related to virus receptors, intracellular trafficking, and productive and nonproductive replication pathways. The end result is that HIV-1 can sequester within the APC for several days and be transmitted via membrane extensions intracellularly and extracellularly to T cells across the virologic synapse. Virus replication requires activated T cells that can develop concurrently with the events of virus transmission. Further research is essential to fill the many gaps in our understanding of these trans infection processes and their role in natural HIV-1 infection.

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“…In this case series, suboptimal compliance with antiretroviral treatment was probably the main cause of poor immune recovery, as proven by frequent episodes of viral replication during follow-up. However, VL itself might play a role: Leishmania co-infection could enhance viral replication and immune activation, thus contributing to CD4 T-cell depletion and increasing the risk of reactivation of latent infections [37],[38]. Thus, even patients with successful antiretroviral treatment could be at risk for Leishmania re-activation.…”

Section: Discussionmentioning

confidence: 99%

Visceral leishmaniasis due to Leishmania infantumwith renal involvement in HIV-infected patients

Vassallo

Moranne

Jeandel³

et al. 2014

BMC Infect Dis

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BackgroundWe describe histological, clinical findings and outcomes of renal involvement during Leishmania infantum infection in four HIV-infected patients in South France and North Italy hospital settings.Cases presentationFour HIV-infected Caucasian patients (age 24-49) performed renal biopsy during episodes of visceral leishmaniasis. They presented severe immunosuppression, frequent relapses of visceral leishmaniasis during a follow-up period of several years and partial or complete recovery of renal function after anti-parasitic treatment. Main clinical presentations were nephrotic or nephritic syndrome and/or acute renal failure secondary to membranoproliferative type III glomerulonephritis or acute interstitial nephritis. Clinical outcome was poor, probably as a consequence of insufficient immuno-virological control of the HIV infection.ConclusionsOur findings suggest that the main histological findings in case of renal involvement due to Leishmania infantum infection in HIV-infected patients are type III MPGN and acute interstitial nephritis, with a histological specificity similar to that observed in canine leishmaniasis. Poor immune status in HIV-infected patients, altering the capacity for parasite clearance, and prolonged course of chronic active VL in this population may lead to the development of specific renal lesions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-014-0561-9) contains supplementary material, which is available to authorized users.

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Mechanisms of interaction between protozoan parasites and HIV

Cited by 32 publications

References 68 publications

Engagement of NKG2D on Bystander Memory CD8 T Cells Promotes Increased Immunopathology following Leishmania major Infection

Engagement of NKG2D on Bystander Memory CD8 T Cells Promotes Increased Immunopathology following Leishmania major Infection

HIV-1TransInfection of CD4⁺T Cells by Professional Antigen Presenting Cells

Visceral leishmaniasis due to Leishmania infantumwith renal involvement in HIV-infected patients

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Mechanisms of interaction between protozoan parasites and HIV

Cited by 32 publications

References 68 publications

Engagement of NKG2D on Bystander Memory CD8 T Cells Promotes Increased Immunopathology following Leishmania major Infection

Engagement of NKG2D on Bystander Memory CD8 T Cells Promotes Increased Immunopathology following Leishmania major Infection

HIV-1TransInfection of CD4+T Cells by Professional Antigen Presenting Cells

Visceral leishmaniasis due to Leishmania infantumwith renal involvement in HIV-infected patients

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Product

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HIV-1TransInfection of CD4⁺T Cells by Professional Antigen Presenting Cells