Tanya L Kowalczyk Mullins1, Su X Li2, James Bethel2, Maureen M Goodenow3, Stephanie Hudey4, John W Sleasman5. 1. Division of Adolescent and Transition Medicine Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave, MLC 4000, Cincinnati, OH, 45229, United States; University of Cincinnati College of Medicine, CARE/Crawley Building, Suite E-870, 3230 Eden Avenue, Cincinnati, OH, 45267, United States. Electronic address: tanya.mullins@cchmc.org. 2. Westat, 1600 Research Boulevard, Rockville, MD, 20850, United States. 3. Dept. of Pathology, Immunology and Laboratory Medicine, University of Florida, College of Medicine, P.O. Box 103633 Gainesville, FL, 32610, United States. 4. Morsani College of Medicine, University of South Florida, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, United States. 5. Duke University, School of Medicine, Department of Pediatrics, 133 MSRB I, DUMC Box 2644, Durham, NC, 27710, United States.
Abstract
BACKGROUND: Human immunodeficiency virus (HIV) infection is associated with chronic immune activation, and concurrent sexually transmitted infections (STIs) may increase immune activation. OBJECTIVES: Because HIV-infected youth are at high risk of STIs and little is known about the impact of STIs on immune activation in HIV-infected youth, we conducted an exploratory study examining the association between STIs and systemic inflammation and immune activation among HIV-infected adolescents. STUDY DESIGN: Forty-nine behaviorally infected U.S. youth ages 18-24 years with baseline CD4+ T-cells >350 who maintained viral suppression on therapy by week 48 were included. Evaluation for STIs (herpes simplex virus [HSV], Chlamydia trachomatis, syphilis, Neisseria gonorrhoeae) was conducted as standard of care and reported on case report forms. Measures of T-cell subsets, systemic immune activation, and soluble factors were examined at week 48 for differences between participants with an STI diagnosis during the 48 weeks compared to those without an STI. RESULTS: Forty-three participants (88%) were male; 57% had baseline CD4+ T-cell counts >500 cells/mm3. Eighteen youth were reported to have ≥1 STI. At week 48, participants with STIs demonstrated lower CD4+ T-cell counts (any STI vs. no STI, p = 0.024; HSV vs. no STI, p = 0.022) and evidence of increased systemic immune activation, including higher CD57 intensity, higher HLA-DR intensity, and lower CD28 percentage, when compared to those without STIs. There were no differences in soluble factors between STI groups. CONCLUSIONS: Results indicate novel activation of CD4+ T-cells among HIV-infected youth who have STIs other than HSV, which may contribute to disease progression.
BACKGROUND:Human immunodeficiency virus (HIV) infection is associated with chronic immune activation, and concurrent sexually transmitted infections (STIs) may increase immune activation. OBJECTIVES: Because HIV-infected youth are at high risk of STIs and little is known about the impact of STIs on immune activation in HIV-infected youth, we conducted an exploratory study examining the association between STIs and systemic inflammation and immune activation among HIV-infected adolescents. STUDY DESIGN: Forty-nine behaviorally infected U.S. youth ages 18-24 years with baseline CD4+ T-cells >350 who maintained viral suppression on therapy by week 48 were included. Evaluation for STIs (herpes simplex virus [HSV], Chlamydia trachomatis, syphilis, Neisseria gonorrhoeae) was conducted as standard of care and reported on case report forms. Measures of T-cell subsets, systemic immune activation, and soluble factors were examined at week 48 for differences between participants with an STI diagnosis during the 48 weeks compared to those without an STI. RESULTS: Forty-three participants (88%) were male; 57% had baseline CD4+ T-cell counts >500 cells/mm3. Eighteen youth were reported to have ≥1 STI. At week 48, participants with STIs demonstrated lower CD4+ T-cell counts (any STI vs. no STI, p = 0.024; HSV vs. no STI, p = 0.022) and evidence of increased systemic immune activation, including higher CD57 intensity, higher HLA-DR intensity, and lower CD28 percentage, when compared to those without STIs. There were no differences in soluble factors between STI groups. CONCLUSIONS: Results indicate novel activation of CD4+ T-cells among HIV-infected youth who have STIs other than HSV, which may contribute to disease progression.
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