HIV and liver disease: a comprehensive update

Abstract

Despite substantial advances in the field, liver disease morbidity and mortality remain serious issues among people with HIV. The causes of liver disease are often multifactorial and include hepatitis viruses, hepatic steatosis and oxidative stress, bacterial translocation with activation of hepatic macrophages and stellate cells, and direct toxicities from alcohol and drugs of abuse. Biopsychosocial factors including a high prevalence of psychiatric disorders, food insecurity, insufficient access to care and medications, and social stigma all play roles in the persistence of liver injury and hepatic fibrosis development among people with HIV. Rising rates of hepatocellular carcinoma have been observed, suggesting that the epidemiology of liver disease is evolving.

Figure 1.

Schematic diagram depicting cytokines and chemokines that modulate hepatic injury and fibrosis. Red arrows indicate chemokine secretion; thick arrows denote pro-inflammatory infiltration.

Figure 2.

Schematic showing potential targets for decreasing liver injury (boxed text) that are not disease specific and may find application in people with HIV. Solid arrows indicate impact on disease pathogenesis; dotted arrows denote gut microbiome metabolite leakage into portal circulation. BCAA, branched-chain amino acid; CYP, cytochrome P450; FGF, fibroblast growth factor; FMT, fecal microbiota transplantation; FXR, farnesoid X receptor; LPS, lipopolysaccharide; SCFA, short-chain fatty acid; TLR, toll-like receptor.

Figure 3.

Diagram summarizing the complex interplay between HIV infection and depression and other manifestations of psychiatric and behavior disease processes. (Diagram courtesy of Glenn Treisman, MD, PhD.)