Pathogenesis of accelerated fibrosis in HIV/HCV co-infection.

Publication Type:



The Journal of infectious diseases, Volume 207 Suppl 1, p.S13-8 (2013)


Apoptosisdigestive disease, digestive deseases Bacterial Translocationdigestive disease, digestive deseases Coinfectiondigestive disease, digestive deseases Cytokinesdigestive disease, digestive deseases Hepatitis Cdigestive disease, digestive deseases HIV Infectionsdigestive disease, digestive deseases Humansdigestive disease, digestive deseases Liver Cirrhosisdigestive disease, digestive deseases Oxidative Stress


Human immunodeficiency virus (HIV) infection is a major cause of acceleration of hepatitis C virus-related liver disease, cirrhosis, and death. However, studies of liver disease pathogenesis in HIV/HCV coinfection have thus far been limited. Emerging data support multiple derangements attending HIV coinfection, including increases in profibrogenic cytokine expression and secretion, generation of enhanced oxidative stress, and increases in hepaotcyte apoptosis. These derangements may be further augmented in the presence of increased microbial translocation in the setting of HIV disease. New insight into the mechanisms of HIV/HCV pathogenesis causing accelerated liver fibrosis could lead to new therapeutic strategies designed to retard ths process.