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Immune cellular parameters of leprosy and human immunodeficiency virus-1 co-infected subjects
Karina I Carvalho1, Solange Maeda, Luciana Marti
1Federal University of São Paulo, São Paulo, Brazil.
Insights
Co-infection with leprosy and human immunodeficiency virus-1 (HIV-1) alters cellular immunity, potentially worsening HIV-1 disease progression. A T helper 2 (Th2) bias is observed in both infections, but not amplified in co-infection.
Area of Science:
- Immunology
- Infectious Diseases
- Virology
Background:
- Interactions between pathogens and host cellular immunity dictate disease manifestations in infections like leprosy and human immunodeficiency virus-1 (HIV-1).
- Co-infection with HIV-1 and Mycobacterium leprae (leprosy) presents a complex interplay of immune responses.
- Understanding these interactions is crucial for managing co-infected individuals and predicting disease outcomes.
Purpose of the Study:
- To explore cellular immunity aspects in patients co-infected with HIV-1 and Mycobacterium leprae.
- To compare immune profiles between co-infected, mono-infected (HIV-1 or M. leprae), and healthy individuals.
- To investigate the impact of co-infection on T-cell subpopulations, activation status, and dendritic cell phenotypes.
Main Methods:
- Study included 28 individuals across four groups: healthy controls, HIV-1 and M. leprae co-infection, HIV-1 mono-infection, and M. leprae mono-infection.
- Peripheral blood mononuclear cells (PBMC) were analyzed using six- and seven-colour flow cytometry.
- Evaluated T-cell subpopulations, activation status, dendritic cell phenotypes, and IL-4 production by T cells.
Main Results:
- Co-infected individuals showed lower CD4:CD8 ratios and higher CD8(+) T-cell activation compared to HIV-1 mono-infected subjects.
- Increased Vδ:Vδ2 T cell ratios and decreased percentages of plasmacytoid dendritic cells were observed in the co-infected group.
- IL-4 production by CD4(+) T lymphocytes correlated positively with effector memory CD4(+) T cells across infected groups, indicating antigen-driven T-cell differentiation.
Conclusions:
- Co-infection with Mycobacterium leprae may exacerbate the immunopathology associated with HIV-1 disease.
- A T helper 2 (Th2) bias in the CD4(+) T-cell response was evident in both HIV-1 infection and leprosy.
- No additive Th2 bias effect was observed in patients co-infected with both HIV-1 and M. leprae.
Abstract:
Leprosy and human immunodeficiency virus-1 (HIV-1) are examples of human infections where interactions between the pathogen and the host cellular immunity determine the clinical manifestations of disease. Hence, a significant immunopathological interaction between HIV-1 and leprosy might be expected. In the present study we explored several aspects of cellular immunity in patients co-infected with HIV-1 and Mycobacterium leprae. Twenty-eight individuals were studied, comprising four groups: healthy controls, HIV-1 and M. leprae co-infection, HIV-1 mono-infection, and M. leprae mono-infection. Subjects in the mono-infection and co-infection groups were matched as far as possible for bacillary load and HIV disease status, as appropriate. Peripheral blood mononuclear cells (PBMC) were analysed using six- and seven-colour flow cytometry to evaluate T-cell subpopulations and their activation status, dendritic cell (DC) distribution phenotypes and expression of IL-4 by T cells. The co-infected group exhibited lower CD4 : CD8 ratios, higher levels of CD8(+) T-cell activation, increased V delta : V delta 2 T cell ratios and decreased percentages of plasmacytoid DC, compared with HIV-1 mono-infected subjects. Across infected groups, IL-4 production by CD4(+) T lymphocytes was positively correlated with the percentage of effector memory CD4(+) T cells, suggesting antigenically driven differentiation of this population of T cells in both HIV-1 and M. leprae infections. Co-infection with M. leprae may exacerbate the immunopathology of HIV-1 disease. A T helper 2 (Th2) bias in the CD4(+) T-cell response was evident in both HIV-1 infection and leprosy, but no additive effect was apparent in co-infected patients.
