Liver fibrosis and accelerated immune dysfunction(immunosenescence) among HIV-infected with heavy alcohol consumption


The Clinical Gastroenterology Journal, is successfully running which covers a wide variety of specialties including digestive system, gastrointestinal diseases, liver, bilary tract, pancreas, diseases of related organs Ulcer medicine, Colitis, Diverticulitis and associated disorders and their treatment. reaching out to analytical scientists worldwide.

Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation.

Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-β1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs.

Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown.

The multifactorial mechanisms driving negative health outcomes among risky drinkers with HIV may include Immunosenescence. Immunosenescence, aging of the immune system, may be accentuated in HIV and leads to poor outcomes.

Heavy alcohol use is more prevalent among people living with human immunodeficiency virus/acquired immunodeficiency syndrome (PLWHA) than among uninfected people and is associated with liver disease and multiple negative health outcomes. Alcohol related liver injury among PLWHA is compounded by high prevalence of liver-related comorbidities occurring among PLWHA such as viral hepatitis. The multifactorial mechanisms driving negative health outcomes among PLWHA who are risky drinkers are still being elucidated.

The liver plays a critical role in metabolic detoxification and immune regulation. It receives blood from the hepatic arteries and the portal venous system. Blood from the portal venous system contains nutrients, metabolic products as well as toxins and antigens. Thus, the liver must balance immune activation from antigen exposure with preventing damage to hepatocytes and surrounding tissues from the antigenic response.

Those with advanced liver fibrosis/cirrhosis had more prevalent hepatitis C co-infection. Among those with Fibroscan data, median Fibroscan scores were higher among those with evidence of liver fibrosis compared to those without. In this exploratory study of ART-naïve PLWHA with heavy drinking, those with advanced liver fibrosis/cirrhosis appeared to have lower prevalence of CD8+ T-cell phenotypes suggestive of immunosenescence (i.e. lower proportions CD8 + CD28-CD57+, higher naïve: memory CD8+ T-cell ratio)

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