74. Association of T Cell Activation with a Non-invasive Marker of Liver Fibrosis in HIV-infected Women with and without Hepatitis C Co-infection
Session: Oral Abstract Session: HIV: Treatment, Complications, and Outcomes
Thursday, October 3, 2013: 8:30 AM
Room: The Moscone Center: 250-262
Background: Liver disease is a common complication of HIV infection, particularly in persons co-infected with hepatitis C virus (HCV). The impact of HIV-associated T cell activation on HIV-associated liver disease in persons with HCV co-infection is not known. 

Methods: Participants in the Women’s Interagency HIV Study (WIHS), a prospective cohort of HIV-infected US women, were studied. Percentages of activated CD4+ and CD8+ T cells expressing HLA-DR and CD38 were measured in 351 co-infected (HIV+HCV+) and 269 mono-infected (HIV+HCV-) women and were correlated with APRI, a non-invasive marker of liver fibrosis. T cell activation markers and APRI were measured at multiple (median: 2; range: 1-8) visits per woman during 1994-2002. Linear regression models with generalized estimating equations were used to evaluate the associations over repeat measures of APRI (the dependent variable, utilizing logarithmic transformation) with percentages of CD4+ or CD8+ activated cells (CD4+ or CD8+ CD38+DR+, categorized into tertiles). 

Results: For both HIV-mono-infected and HCV co-infected women, increased APRI was associated with higher plasma HIV RNA and lower CD4 count (both p-trend <0.001).  Among co-infected women, increased APRI was also associated with higher baseline HCV RNA (p<0.001).  Among co-infected women, higher percentage of activated CD4+ cells was positively associated with APRI (p-trend=0.003) after adjusting for race/ethnicity, baseline HCV RNA, and HIV RNA, but not after adjusting for CD4+ count (p=0.14).  Higher percentage of activated CD8 cells was not associated with APRI after adjustment for covariates.   Among mono-infected women, the positive association of APRI with CD4+ activation was borderline (p=0.06) but significant for CD8+ cells (p=0.01) after adjusting for race/ethnicity and HIV RNA.  The association of APRI with CD8+ activated cells remained after adjustment for CD4+ count (p=0.04) but not with CD4+ activated cells (p=0.28).

Conclusion: T cell activation is associated with markers of liver fibrosis in HIV-infected women, independent of HIV RNA level. Targeted treatments to reduce T cell activation could be evaluated to reduce incidence of liver fibrosis in HIV mono-infected and possibly HCV co-infected patients. 

Eva Operskalski, PhD1, Roksana Karim, PhD, MBBS2, Shawna Christensen, MS3, Wendy J. Mack, PhD4, Toni Frederick, PhD5, Jiaao Xu, MBBS3, Barbara Weiser, MD6, Harold Burger, PhD, MD6, Mark H. Kuniholm, PhD7, Brian Edlin, MD8, Chenglong Liu, MD, PhD9, Marion G. Peters, MD10, Audrey French, MD11, Elizabeth T. Golub, PhD12, Gerald B. Sharp, DrPH13 and Andrea Kovacs, MD14, (1)Pediatrics, University of Southern California, Los Angeles, CA, (2)Research Pediatrics, Keck School of Medicine of USC, Los Angeles, CA, (3)University of Southern California, Los Angeles, CA, (4)Preventive Medicine, Keck School of Medicine at USC, Los Angeles, CA, (5)Research Pediatrics, University of Southern California, Los Angeles, CA, (6)Sacramento VA Medical Center, Mather, CA, (7)Department Of Epidemiology & Population Health, Albert Einstein College of Medicine, Bronx, NY, (8)SUNY Downstate College of Medicine, Brooklyn, NY, (9)Georgetown University Medical Center, Washington, DC, (10)University of California, San Francisco, CA, (11)John H. Stroger, Jr. Hospital of Cook County, Chicago, IL, (12)Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, (13)National Institutes of Health, Bethesda, MD, (14)Pediatrics, Keck School of Medicine at USC, Los Angeles, CA


E. Operskalski, None

R. Karim, None

S. Christensen, None

W. J. Mack, None

T. Frederick, None

J. Xu, None

B. Weiser, None

H. Burger, None

M. H. Kuniholm, None

B. Edlin, None

C. Liu, None

M. G. Peters, None

A. French, None

E. T. Golub, None

G. B. Sharp, None

A. Kovacs, None

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