Brandilyn A Peters1, Lila A Sheira2, David B Hanna1, Qibin Qi1, Anjali Sharma3, Adebola Adedimeji1, Tracey Wilson4, Daniel Merenstein5, Phyllis C Tien6,7, Mardge Cohen8, Eryka L Wentz9, Jennifer Kinslow10, Alan L Landay10, Sheri D Weiser2,6,11. 1. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, USA. 2. Division of HIV, Infectious Diseases, and Global Medicine, University of California, San Francisco, San Francisco, California, USA. 3. Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA. 4. Department of Community Health Sciences, SUNY Downstate Health Sciences University, School of Public Health, Brooklyn, New York, USA. 5. Department of Medicine, Georgetown University Medical Center, Washington, DC, USA. 6. Department of Medicine, University of California San Francisco, San Francisco, California, USA. 7. Department of Veterans Affairs Medical Center, San Francisco, California, USA. 8. Department of Medicine, Cook County Health and Hospital System, Chicago, Illinois, USA. 9. Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA. 10. Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois, USA. 11. Center for AIDS Prevention Studies, University of California, San Francisco, San Francisco, California, USA.
Abstract
BACKGROUND: Food insecurity is associated with increased morbidity and mortality in people with human immunodeficiency virus (HIV) on antiretroviral therapy, but its relationship with immune dysregulation, a hallmark of HIV infection and comorbidity, is unknown. METHODS: In 241 women participating in the Women's Interagency HIV Study, peripheral blood mononuclear cells were characterized by flow cytometry to identify cell subsets, comprising surface markers of activation (%CD38+HLADR+), senescence (%CD57+CD28-), exhaustion (%PD-1+), and co-stimulation (%CD57- CD28+) on CD4+ and CD8+ T cells. Mixed-effects linear regression models were used to assess the relationships of food insecurity with immune outcomes, accounting for repeated measures at ≤3 study visits and adjusting for sociodemographic and clinical factors. RESULTS: At the baseline study visit, 71% of participants identified as non-Hispanic Black, 75% were virally suppressed, and 43% experienced food insecurity. Food insecurity was associated with increased activation of CD4+ and CD8+ T cells, increased senescence of CD8+ T cells, and decreased co-stimulation of CD4+ and CD8+ T cells (all P < .05), adjusting for age, race/ethnicity, income, education, substance use, smoking, HIV viral load, and CD4 count. In stratified analyses, the association of food insecurity with CD4+ T-cell activation was more pronounced in women with uncontrolled HIV (viral load >40 copies/mL and CD4 <500 cells/mm3) but remained statistically significant in those with controlled HIV. CONCLUSIONS: Food insecurity may contribute to the persistent immune activation and senescence in women with HIV on antiretroviral therapy, independently of HIV control. Reducing food insecurity may be important for decreasing non-AIDS-related disease risk in this population.
BACKGROUND: Food insecurity is associated with increased morbidity and mortality in people with human immunodeficiency virus (HIV) on antiretroviral therapy, but its relationship with immune dysregulation, a hallmark of HIV infection and comorbidity, is unknown. METHODS: In 241 women participating in the Women's Interagency HIV Study, peripheral blood mononuclear cells were characterized by flow cytometry to identify cell subsets, comprising surface markers of activation (%CD38+HLADR+), senescence (%CD57+CD28-), exhaustion (%PD-1+), and co-stimulation (%CD57- CD28+) on CD4+ and CD8+ T cells. Mixed-effects linear regression models were used to assess the relationships of food insecurity with immune outcomes, accounting for repeated measures at ≤3 study visits and adjusting for sociodemographic and clinical factors. RESULTS: At the baseline study visit, 71% of participants identified as non-Hispanic Black, 75% were virally suppressed, and 43% experienced food insecurity. Food insecurity was associated with increased activation of CD4+ and CD8+ T cells, increased senescence of CD8+ T cells, and decreased co-stimulation of CD4+ and CD8+ T cells (all P < .05), adjusting for age, race/ethnicity, income, education, substance use, smoking, HIV viral load, and CD4 count. In stratified analyses, the association of food insecurity with CD4+ T-cell activation was more pronounced in women with uncontrolled HIV (viral load >40 copies/mL and CD4 <500 cells/mm3) but remained statistically significant in those with controlled HIV. CONCLUSIONS: Food insecurity may contribute to the persistent immune activation and senescence in women with HIV on antiretroviral therapy, independently of HIV control. Reducing food insecurity may be important for decreasing non-AIDS-related disease risk in this population.
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