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An In Vitro Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection
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Mtb/HIV co-infection immune microenvironment subpopulations heterogeneity
Jiamin Gao1, Xianzhen Huang1, Qingdong Zhu1
1Laboratory of Infectious Disease, HIV/AIDS Clinical Treatment Center of Guangxi (Nanning) and The Fourth People's Hospital of Nanning, Nanning 530023, China; Department of Tuberculosis, The Fourth People's Hospital of Nanning, Nanning 530023, China.
International Immunopharmacology
|October 15, 2024
Summary
Dual infection with tuberculosis (TB) and human immunodeficiency virus (HIV) causes significant immune cell changes. This study reveals immune cell heterogeneity in TB/HIV co-infection, impacting immune dysfunction.
Area of Science:
- Immunology
- Genomics
- Infectious Diseases
Background:
- Co-infection with human immunodeficiency virus type 1 (HIV-1) and tuberculosis (TB) presents a critical health challenge.
- Current understanding of immune responses and cellular heterogeneity in dual infections is limited.
Purpose of the Study:
- To investigate the cellular heterogeneity and immune responses in individuals co-infected with Mycobacterium tuberculosis (Mtb) and HIV.
- To identify specific immune cell subpopulations and their roles in the progression of Mtb/HIV co-infection.
Main Methods:
- Utilized single-cell RNA sequencing data from public databases (Gene Expression Omnibus, China National GeneBank Nucleotide Sequence Archive).
- Analyzed peripheral blood mononuclear cells (PBMCs) from HIV-1 infected and Mtb/HIV co-infected individuals.
- Investigated cellular components, signaling pathways, biological functions, developmental trajectories, and gene regulatory networks.
Main Results:
- Generated a single-cell transcriptional landscape of Mtb/HIV co-infection, highlighting cellular heterogeneity.
- Identified CD4+ T_RACK1_STAT1 and CD8+ T_RACK1_TIGIT subpopulations potentially involved in immune regulation and T cell function.
- Discovered monocyte subpopulations (Mono_HSP90AA1, Mono_APOBEC3A) at differentiation endpoints and enriched cytotoxic T lymphocyte (CTL_GNLY) and natural killer (NK_HSPA1A) subpopulations in HIV-infected groups.
Conclusions:
- HIV-1 infection exacerbates immune disruptions when co-infected with Mtb.
- Mtb/HIV co-infection leads to significant immune cell subpopulation heterogeneity, contributing to immune dysfunction.
