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Open Forum Infect Dis. 2018 Jun 11;5(7):ofy138. doi: 10.1093/ofid/ofy138. eCollection 2018 Jul.

Markers of Tissue Repair and Cellular Aging Are Increased in the Liver Tissue of Patients With HIV Infection Regardless of Presence of HCV Coinfection.

Author information

1
Duke University School of Medicine, Durham, North Carolina.
2
Duke Clinical Research Institute, Durham, North Carolina.
3
Medical University of South Carolina, Charleston, South Carolina.
4
Durham VA Medical Center, Durham, North Carolina.
5
University of North Carolina School of Medicine, Chapel Hill, North Carolina.
6
Ralph H. Johnson VA Medical Center, Charleston, South Carolina.

Abstract

Liver disease is a leading cause of HIV-related mortality. Hepatitis C virus (HCV)-related fibrogenesis is accelerated in the setting of HIV coinfection, yet the mechanisms underlying this aggressive pathogenesis are unclear. We identified formalin-fixed paraffin-embedded liver tissue for HIV-infected patients, HCV-infected patients, HIV/HCV-coinfected patients, and controls at Duke University Medical Center. De-identified sections were stained for markers against the wound repair Hedgehog (Hh) pathway, resident T-lymphocytes, and immune activation and cellular aging. HIV infection was independently associated with Hh activation and markers of immune dysregulation in the liver tissue.

KEYWORDS:

GLI; Hedgehog; Sonic Hedgehog; fibrogenesis; hepatitis C virus; human immunodeficiency virus; patched; pathogenesis; wound repair

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