Elevated Inflammation Associated with Markers of Neutrophil Function and Gastrointestinal Disruption in Pilot Study of Plasmodium fragile Co-Infection of ART-Treated SIVmac239+ Rhesus Macaques

Human immunodeficiency virus (HIV) and malaria, caused by infection with spp., are endemic in similar geographical locations. As a result, there is high potential for HIV/ co-infection, which increases the pathology of both diseases. However, the immunological mechanisms underlying the exacerbated d...

Full description

Saved in:

Bibliographic Details
Published in:	Viruses Vol. 16; no. 7; p. 1036
Main Authors:	Nemphos, Sydney M, Green, Hannah C, Prusak, James E, Fell, Sallie L, Goff, Kelly, Varnado, Megan, Didier, Kaitlin, Guy, Natalie, Moström, Matilda J, Tatum, Coty, Massey, Chad, Barnes, Mary B, Rowe, Lori A, Allers, Carolina, Blair, Robert V, Embers, Monica E, Maness, Nicholas J, Marx, Preston A, Grasperge, Brooke, Kaur, Amitinder, De Paris, Kristina, Shaffer, Jeffrey G, Hensley-McBain, Tiffany, Londono-Renteria, Berlin, Manuzak, Jennifer A
Format:	Journal Article
Language:	English
Published:	Switzerland MDPI AG 01-07-2024
Subjects:	Anemia Animal welfare Animals Anti-Retroviral Agents - therapeutic use Antibiotics Antiparasitic agents Antiretroviral therapy Antiviral agents Biomarkers - blood Blood Care and treatment CD4 antigen co-infection Coinfection - drug therapy Coinfection - parasitology Coinfection - virology Cytokines - blood Degranulation Disease Models, Animal Disease transmission Dosage and administration Drug resistance Elastase Health aspects HIV HIV infection HIV Infections - complications HIV Infections - drug therapy HIV Infections - immunology Human immunodeficiency virus Immune system Infections Inflammation Laboratory animals Leukocytes (neutrophilic) Lymphocytes T Macaca mulatta Malaria Malaria - complications Malaria - drug therapy Malaria - immunology Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes Mortality Neutrophils Neutrophils - immunology nonhuman primate Parasitemia Pathogenesis Pathology Physiological aspects Pilot Projects Plasmodium Plasmodium falciparum Plasmodium fragile Simian Acquired Immunodeficiency Syndrome - complications Simian Acquired Immunodeficiency Syndrome - drug therapy Simian Acquired Immunodeficiency Syndrome - immunology Simian Immunodeficiency Virus Viral Load United States United States > US simian immunodeficiency virus co-infection Plasmodium fragile nonhuman primate malaria immunology neutrophils
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Human immunodeficiency virus (HIV) and malaria, caused by infection with spp., are endemic in similar geographical locations. As a result, there is high potential for HIV/ co-infection, which increases the pathology of both diseases. However, the immunological mechanisms underlying the exacerbated disease pathology observed in co-infected individuals are poorly understood. Moreover, there is limited data available on the impact of co-infection on antiretroviral (ART)-treated HIV infection. Here, we used the rhesus macaque (RM) model to conduct a pilot study to establish a model of co-infection during ART-treated simian immunodeficiency virus (SIV) infection, and to begin to characterize the immunopathogenic effect of co-infection in the context of ART. We observed that co-infection resulted in parasitemia and anemia, as well as persistently detectable viral loads (VLs) and decreased absolute CD4+ T-cell counts despite daily ART treatment. Notably, co-infection was associated with increased levels of inflammatory cytokines, including monocyte chemoattractant protein 1 (MCP-1). co-infection was also associated with increased levels of neutrophil elastase, a plasma marker of neutrophil extracellular trap (NET) formation, but significant decreases in markers of neutrophil degranulation, potentially indicating a shift in the neutrophil functionality during co-infection. Finally, we characterized the levels of plasma markers of gastrointestinal (GI) barrier permeability and microbial translocation and observed significant correlations between indicators of GI dysfunction, clinical markers of SIV and infection, and neutrophil frequency and function. Taken together, these pilot data verify the utility of using the RM model to examine ART-treated SIV/ co-infection, and indicate that neutrophil-driven inflammation and GI dysfunction may underlie heightened SIV/ co-infection pathogenesis.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1999-4915 1999-4915
DOI:	10.3390/v16071036