Gastroenterology
Volume 137, Issue 3 , Pages 795-814, September 2009

Coinfection With HIV-1 and HCV—A One-Two Punch

  • Arthur Y. Kim

      Affiliations

    • Division of Infectious Diseases and the Ragon Institute of MGH, MIT, and Harvard (formerly known as the Partners AIDS Research Center), Massachusetts General Hospital, Boston, Massachusetts
    • Corresponding Author InformationReprint requests Address requests for reprints to: Arthur Y. Kim, MD, Massachusetts General Hospital, Cox 5, 55 Fruit Street, Boston, Massachusetts 02114
  • ,
  • Raymond T. Chung

      Affiliations

    • Gastrointestinal Unit, Massachusetts General Hospital, Boston, Massachusetts
    • Corresponding Author InformationReprint requests Address requests for reprints to: Raymond T. Chung, MD, Massachusetts General Hospital, Warren 1007, 55 Fruit Street, Boston, Massachusetts 02114

Received 6 April 2009; accepted 13 June 2009. published online 22 June 2009.

John P. Lynch and David C. Metz, Section Editors

Hepatitis C virus (HCV) infection is a major cause of chronic liver disease, cirrhosis, and death; it is estimated that 180 million persons are infected with HCV worldwide. The consequences of HCV are worse in those who are coinfected with human immunodeficiency virus 1 (HIV-1), which is unfortunately a common scenario because of shared risk factors of the viruses. More studies into effects of HCV/HIV-1 coinfection are needed, but efforts have been hampered by limitations in our understanding of the combined pathogenesis of the 2 viruses. Gaining insight into the mechanisms that underlie the immunopathogenesis of these persistent viral infections could lead to new therapeutic strategies for patients with HCV/HIV-1 coinfection.

Abbreviations used in this paper: AIDS, acquired immune deficiency syndrome, FOXP3, forkhead box P3, HIV-1, human immunodeficiency virus 1, IFN, interferon, IL, interleukin, LPS, lipopolysaccharide, MSM, men who have sex with men, NK, natural killer, NKT cell, natural killer T cell, PD-1, programmed death 1, SIV, simian immunodeficiency virus, TGF, transforming growth factor, Th, T helper, TLR, Toll-like receptor (TLR), TRAIL, tumor necrosis factor–related apoptosis-inducing ligand

 

 Conflicts of interest The authors disclose the following: R.T.C. receives research grant support from Roche Labs and Schering-Plough. A.Y.K. discloses no conflicts.

 Funding Supported by National Institutes of Health grants U19 AI066345 and K23 AI054379 (to A.Y.K.) and National Institutes of Health grants R01 AI069939 and K24 DK078772-02 (to R.T.C.).

PII: S0016-5085(09)00997-4

doi:10.1053/j.gastro.2009.06.040

Gastroenterology
Volume 137, Issue 3 , Pages 795-814, September 2009