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Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
Published on: September 1, 2015
Studies on the allostimulatory function of dendritic cells from HCV-HIV-1 co-infected patients
Justin Stebbing1, Steve Patterson, Simon Portsmouth
1The Department of Immunology, Division of Investigative Science, Faculty of Medicine, Imperial College of Science, Technology and Medicine, The Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH,UK. j.stebbing@imperial.ac.uk
Insights
HIV-1 and hepatitis C (HCV) co-infection did not significantly impair dendritic cell (DC) function compared to HIV-1 infection alone. This suggests HCV co-infection may not alter HIV disease progression or impact immunotherapies.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- HIV-1 and Hepatitis C Virus (HCV) co-infection is associated with significant health risks.
- HCV is known to impair dendritic cell (DC) function, but its effect on DC function in the context of HIV-1 co-infection is unclear.
- Previous studies suggest HCV co-infection may not alter HIV disease progression.
Purpose of the Study:
- To investigate the effect of HIV-1 and HCV co-infection on monocyte-derived dendritic cell (DC) allostimulatory capacity.
- To compare DC function in co-infected individuals with that of HIV-1-infected individuals without HCV.
- To explore the impact of Th1 cytokines on DC function in co-infected individuals.
Main Methods:
- Monocyte-derived DCs were generated from HIV-1 positive individuals with and without HCV co-infection, matched for CD4 count, viral load, and therapy.
- Mixed leukocyte reactions were performed to assess DC allostimulatory capacity.
- Thymidine uptake and CFSE cell division analyses were used to measure DC function, with and without exogenous Th1 cytokines (IL-2, IL-12).
Main Results:
- Monocyte-derived DCs from HIV-1 and HCV co-infected individuals exhibited no significant difference in allostimulatory capacity compared to DCs from HIV-1 infected individuals without HCV.
- The impairment of DC allostimulatory capacity observed in HCV infection alone was not reversed by IL-2 or IL-12 in co-infected individuals.
- DC function in co-infected individuals was comparable to that in matched HIV-1-infected patients without HCV.
Conclusions:
- HIV-1 and HCV co-infection does not appear to further impair monocyte-derived DC allostimulatory capacity beyond that seen in HIV-1 infection alone.
- These findings support clinical observations that HCV co-infection may not significantly alter HIV disease progression.
- The results have implications for the development of immunotherapeutic strategies for co-infected individuals.
Abstract:
There is increasing recognition of the potential morbidity and mortality associated with HIV-1 and hepatitis C (HCV) co-infection. HIV appears to adversely affect HCV disease while the reciprocal effect of HCV on HIV remains controversial. We therefore studied the effect of co-infection on dendritic cell function versus HIV infection alone, as previous work has shown that HCV impairs dendritic cell (DC) function. HIV-1 positive individuals with HCV were matched for CD4 count, HIV-1 RNA viral load and therapy, to HIV-1 positive patients without HCV. Monocyte-derived DC were generated and mixed leukocyte reactions were performed. We assessed allostimulatory capacity with and without administration of exogenous Th1 cytokines, using thymidine uptake and cell division analyses with the vital dye CFSE. We found that monocyte-derived DC from co-infected individuals showed no significant differences in allostimulatory capacity to ex vivo generated DC from HIV-1 infected individuals without HCV. Unlike the situation with HCV infection alone, this impairment was not reversed by increasing concentrations of either interleukin-2 or -12. Monocyte-derived DC from HIV-1 and HCV co-infected individuals have a similar allostimulatory capacity to DC from matched patients with HIV-1 alone. These findings are compatible with results of prior clinical studies that found no evidence that HCV co-infection altered HIV disease progression and has implications for immunotherapeutic approaches in co-infected individuals.
