Individuals with HIV and hepatitis C virus coinfection show significantly higher levels of particular inflammatory cytokines linked to liver damage, according to a study published online in HIV Medicine.
Researchers examined a range of markers of systemic inflammation in 79 HIV-infected patients – 42 of whom were coinfected with hepatitis C – and all of whom had been on antiretroviral therapy and had plasma viral levels suppressed below 50 HIV-1 RNA copies per ml, and compared them to 20 healthy controls.
Their analysis initially revealed that the individuals with HIV/HCV coinfection had higher plasma levels of interleukin-6, interferon gamma-induced protein (IP)-10, monocyte/macrophage markers neopterin and sCD163, and soluble tumour necrosis factor receptor-II than individuals with HIV infection alone.
However after adjusting for duration of HIV infection and gender, researchers only found a significant difference between HIV/HCV coinfected individuals and those with HIV alone in plasma levels of IP-10, sCD163 and neopterin (HIV Medicine. 2016 May 17. doi:10.1111/hiv.12357).
The study also undertook to correlate these markers with hepatic damage, and found a highly significant and consistent relationship between aspartate aminotransferase, alanine aminotransferase and AST-to platelet-ratio index, and plasma IP-10, sCD163 and neopterin.
“Although a contribution of ART-induced hepatotoxicity in the setting of HCV/HIV coinfection cannot be excluded, a simpler and more plausible explanation is that the observed effects are related to HCV/HIV-mediated liver damage,” wrote Dr. Konstantin V. Shmagel, from the Institute of Ecology and Genetics of Microorganisms at the Russian Academy of Sciences in Perm, Russia.
“The relationship among these indices remains incompletely understood but it is possible that processes taking place in the liver may play a role in alteration of CD4 T-cell recovery during ART in the setting of HCV/HIV coinfection.”
The analysis also showed the inflammatory markers IL-6, neopterin and sCD14 were also elevated – although not to the same degree – in individuals with HIV monoinfection compared to the healthy controls.
“The drivers of persistent inflammation in treated HIV infection and HIV/HCV coinfection are not entirely clear but, in these settings, damage to the gut epithelial barrier has been implicated in promoting translocation of microbial products from the gut lumen into the systemic circulation,” the authors wrote.
This study was supported by the National Institute of Allergy and Infectious Diseases, the Center for AIDS Research at Case Western Reserve University, and the Russian Science Foundation. No conflicts of interest were declared.