Persistent portal hypertension, a critical factor in advanced liver cirrhosis outcomes, often remains even after a Hepatitis C virus (HCV) cure. A recent study followed 41 adults with advanced HCV-related cirrhosis who achieved a cure with direct-acting antiviral therapy. The research focused on changes in the hepatic venous pressure gradient (HVPG), a key indicator of portal hypertension, over 48 weeks. Investigators analyzed immune profiles at baseline to understand factors influencing HVPG improvement.
The study identified two distinct immunological profiles linked to unresolved portal hypertension, differing significantly based on HIV status.
In patients without HIV, a lack of improvement in HVPG correlated with a broader inflammatory response, including elevated levels of TNF-α, IL-17A, and IL-10. This was also associated with widespread CD4+ T cell activation.
For patients with HIV, impaired HVPG regression was linked to a different pattern. This included markers of endothelial dysfunction such as sVCAM-1, and a more focused CD4+ T cell activation within specific subsets.
These findings suggest that HIV coinfection may alter the body's recovery pathways after an HCV cure, shifting the focus from systemic inflammation to endothelial dysfunction and T cell exhaustion. Understanding these baseline immune signatures could help stratify residual risk and develop targeted treatments for more complete hemodynamic recovery in advanced cirrhosis.