Exploring the Link Between Steatosis Progression and HIV & HCV Infection
Not much is known about how HIV mono-infection contributes to the development of hepatic steatosis, due to how difficult diagnosis of this condition used to be. Now, with the developement of noninvasive tools, it is easier to diagnose steatosis.
A manuscript accepted for publication in the Journal of Hepatology by principal investigator Giada Sebastiani, MD, sought to examine the link between steatosis in HIV mono-infected individuals as well as in those coinfected with HIV and HCV.
Steatosis, also known as fatty liver disease, is a condition where fat accumulates in the liver. When this condition progresses and leads to inflammation, it becomes known as steatohepatitis, which can lead to liver cirrhosis and liver cancer. Steatosis is common in patients who are coinfected with the hepatitis C virus (HCV) and the human immunodeficiency virus (HIV). However, studies examining the contribution of HIV alone on the development of hepatic steatosis are extremely limited.
This type of study was difficult to implement previously as invasive liver biopsies were the standard way to diagnose steatosis. However, with the introduction of new, noninvasive tools to measure and diagnose steatosis such as transient elastography (TE), which measures liver stiffness, and controlled attenuation parameter (CAP), Dr. Sebastiani and her colleagues were able to conduct this study.
The authors established the LIVEr disease in HIV (LIVEHIV) cohort in 2013 at McGill University Health Center where patients were able to undergo screening for liver disease using TE and CAP. The patients included in the study had to be infected with HIV and be at least 18 years old. Of the 726 HIV-infected patients included in the study, 36.4% of them had hepatic steatosis and 29.2% had significant liver cirrhosis. The authors report that the prevalence of hepatic steatosis in HIV mono-infected individuals was found to be 36.1%, while the prevalence of steatosis in those coinfected with HIV and HCV was found to be 38.6%. Both these figures are higher than the prevalence of steatosis in the uninfected general Canadian population, which is between 20% and 25%.
Interestingly, the authors found that patients infected with HIV alone had higher rates of steatosis progression than patients with coinfected with HIV and HCV. This was particularly true in HIV patients who were overweight.
The authors note that the mechanisms leading to hepatic steatosis are different in those only infected with HIV in comparison to those coinfected with HIV and HCV. Potential mechanisms of HIV mono-infection include direct effects of the virus on the formation of fat, long-term effects of antiretroviral therapy, as well as chronic inflammation due to infection. Overall, it appears that HIV infection promotes steatosis by affecting metabolic factors, which is evidenced by the correlation of higher body mass index and triglycerides with the prevalence of steatosis.
This study was the first prospective study to examine the prevalence of hepatic steatosis and its progression to fibrosis in HIV mono-infected patients. In addition, the study demonstrated that HIV mono-infected individuals with higher BMIs are particularly at risk for hepatic steatosis progression and should be monitored for possible interventions. However, the authors acknowledge multiple limitations of the study including lack of an additional method to confirm hepatic steatosis, such as histology or MRI spectroscopy. In addition, the study did not have a long follow-up period, which prohibited the authors from examining the effect of antiretroviral therapy on steatosis and progression to liver cirrhosis.
Samar Mahmoud graduated from Drew University in 2011 with a BA in Biochemistry and Molecular Biology. After two years of working in industry as a Quality Control Technician for a blood bank, she went back to school and graduated from Montclair State University in 2016 with an MS in Pharmaceutical Biochemistry. She is currently pursuing her PhD in Molecular and Cellular Biology at the University of Massachusetts at Amherst.