Genotype distribution in relation to viral load in a large cohort of Indian patients with chronic hepatitis C virus infection: A retrospective analysis.

INTRODUCTION: Hepatitis C virus (HCV) displays high genetic diversity, characterized by regional variations in the prevalence of genotype posing challenges to the development of vaccines and definitive treatment. Very few reports exist on the distribution and frequency change of HCV genotypes in India. In the present retrospective study, we aimed to understand the distribution pattern of HCV genotypes and viral load among HCV-infected patients attending the Asian Institute of Gastroenterology, Hyderabad, India, a tertiary care hospital. METHODS: Patients referred to the Hepatology Department from January 2009 to December 2015 were screened for this study. Eight hundred and sixty-two chronic HCV patients were included in this study. Genotyping was performed using type-specific probe-based hybridization assay and viral load was estimated by real-time polymerase chain reaction. RESULTS: Out of 862 patients, genotype 1 was detected predominantly in 392 (45.5%), followed by genotype 3 in 344 (39.9%) patients; genotypes 4, 6, and 2 were detected in 115 (13.3%), 8 (0.9%), and 3 (0.3%) patients, respectively. The number of patients having genotype 1 increased in frequency while genotype 3 became less from the year 2009 to 2015. Patients having genotype 1 had significantly (p < 0.0001) higher viral load compared with the patients infected with other genotypes. CONCLUSION: Our study results demonstrate a change in HCV genotypic distribution pattern from genotypes 3 to 1 during the span of 7 years in patients referred to our hospital. In the light of the reported difference in the pathogenic potential of various HCV genotypes, detection of HCV genotype appears to be still essential for better patient management.

Identification of circulating CD90 CD73 cells in cirrhosis of liver.

AIM: To identify circulating CD90(+) CD73(+) CD45(-) cells and evaluate their in vitro proliferating abilities. METHODS: Patients with cirrhosis (n = 43), and healthy volunteers (n = 40) were recruited to the study. Mononuclear cells were isolated and cultured from the peripheral blood of controls and cirrhosis patients. Fibroblast-like cells that appeared in cultures were analyzed for morphological features, enumerated by flow cytometry and confirmed by immunocytochemistry (ICC). Colony forming efficiency (CFE) of these cells was assessed and expressed as a percentage. RESULTS: In comparison to healthy volunteers, cells obtained from cirrhotic patients showed a significant increase (P < 0.001) in the percentage of CD90(+) CD73(+) CD45(-) cells in culture. Cultured cells also showed 10 fold increases in CFE. Flow cytometry and ICC confirmed that the proliferating cells expressed CD90(+) CD73(+) in the cultures from cirrhosis patients. CONCLUSION: These results indicate the presence of circulating CD90(+) CD73(+) CD45(-) cells in patients with liver cirrhosis that have the potential to proliferate at a higher rate.

Visceral adipose tissue visfatin in nonalcoholic fatty liver disease.

BACKGROUND: Visfatin is a novel adipocytokine predominantly expressed and secreted by visceral adipose tissue. It is realized for its multiple functions of central importance in NAD biosynthesis, innate immunity and inflammation. Its phosphoribosyl transferase activity regulates cellular energetics and NAD dependent enzymes such as SIRTUINS. Although its expression in various tissues and circulating levels are documented, visceral visfatin levels in Nonalcoholic fatty liver disease (NAFLD) patients have not been reported. OBJECTIVE: The aim of the present study was to assess visceral adipose tissue visfatin levels in NAFLD. Materials and methods. A total of 115 patients undergoing diagnostic laparoscopy were recruited in the study and categorized into two groups based on standard criteria for NAFLD. Visceral adipose tissue TNF-a, IL-6 and visfatin levels were measured by ELISA. Blood glucose, lipids, liver enzymes and non esterified fatty acids (NEFA) were estimated using standard procedures. Formalin fixed, Hematoxylene Eosin stained liver biopsy specimens were examined for the presence of steatosis and the degree of steatosis was ascertained as per Brunt.s classification. RESULTS: The visceral visfatin level declined significantly (P < 0.001) in all groups of NAFLD as compared to non NAFLD group, while plasma NEFA level increased with progressive steatosis (P < 0.02). Significant increase in TNF a was observed in all groups of NAFLD, while IL-6 increased in NASH only. CONCLUSION: A significant decline in visceral adipose tissue visfatin level was found to be associated with degree of steatosis in NAFLD patients.