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HIV infection is associated with higher levels of monocyte chemoattractant protein-1 and eotaxin among people with recent hepatitis C virus infection.

Lamoury FM, Hajarizadeh B, Keoshkerian E, Feld JJ, Amin J, Teutsch S, Matthews GV, Hellard M, Dore GJ, Lloyd AR, Applegate TL, Grebely J and the ATAHC Study Group.
The Kirby Institute, UNSW Australia, Sydney, Australia. [email protected]


BACKGROUND: Human immunodeficiency virus (HIV) infection leads to more rapid progression of hepatitis C virus (HCV)-related liver fibrosis, which could be linked to differences in the severity of liver inflammation among HIV/HCV co-infected individuals compared to HCV mono-infected individuals. This study assessed the association of HIV co-infection with pro-inflammatory and pro-fibrogenic cytokines and chemokines during recent HCV infection. METHODS: Participants from the ATAHC study, a prospective cohort of recent HCV infection, with detectable HCV RNA at the time of acute HCV detection were included. Concentrations of 27 plasma cytokines and chemokines were measured by multiplex immunoassays and compared between those with, and without, HIV co-infection. RESULTS: Out of 117 individuals with recent HCV infection included in analysis, 73 had HCV mono-infection and 44 had HIV/HCV co-infection. Individuals with HIV/HCV co-infection had significantly higher mean levels of eotaxin (1.79 vs. 1.62 log pg/mL; P < 0.001), monocyte chemotactic protein 1 (MCP-1; 2.10 vs. 1.98 log pg/mL; P < 0.001), and interferon-gamma inducible protein-10 (IP-10; 3.11 vs. 2.98 log pg/mL; P = 0.013). Linear regression analyses adjusting for age, alanine transaminase (ALT), HCV RNA levels, and assay run, higher eotaxin levels were independently associated with HIV/HCV co-infection (adjusted beta: 0.12; 95%CI: 0.01, 0.24; P = 0.039). Higher MCP-1 levels were also independently associated with HIV/HCV co-infection in adjusted analysis (adjusted beta: 0.11; 95%CI: 0.03, 0.18; P = 0.009). CONCLUSIONS: During recent HCV, those with HIV/HCV co-infection had a stronger pro-fibrogenic mediator profile compared to those with HCV mono-infection. These findings may provide a potential explanation for accelerated liver fibrosis in HIV/HCV co-infection. TRIAL REGISTRATION: Australian Trial in Acute Hepatitis C (ATAHC) study was registered with registry on September 11, 2005. NCT00192569 .

This work was supported by the National Health and Medical Research Council (NHMRC) grant HIV and HCV vaccines and immunopathogenesis (#510448) and UNSW Goldstar research grant. The ATAHC study was supported by the National Institutes of Health (#RO1 DA 15999–01). The Kirby Institute is funded by the Australian Government Department of Health and Ageing and is affiliated with the Faculty of Medicine, UNSW Australia. GD is recipient of the NHMRC practitioner fellowship. JG is recipient of the NHMRC Career Development Fellowship

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  • Journal: BMC Infectious Diseases
  • Published: 01/06/2016
  • Volume: 16
  • Issue: 1
  • Pagination: 241