Send to

Choose Destination
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

Duke University School of Medicine, Durham, North Carolina.
Duke Clinical Research Institute, Durham, North Carolina.
Medical University of South Carolina, Charleston, South Carolina.
Durham VA Medical Center, Durham, North Carolina.
University of North Carolina School of Medicine, Chapel Hill, North Carolina.
Ralph H. Johnson VA Medical Center, Charleston, South Carolina.


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.


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

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for PubMed Central
Loading ...
Support Center