https://www.gastrojournal.org/article/S0016-5085(03)50023-3/pdf

Progression of fibrosis in chronic hepatitis C

Natural History of Hepatitis C

[Non-A, non-B viral hepatitis].

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.1840360708

Noninvasive monitoring of patients with chronic hepatitis C

Chronic hepatitis C, attributed to infection with hepatitis C virus (HCV), is a global health problem. The overall prevalence of viral hepatitis worldwide is estimated to be 3-5% with over 175 million people infected with HCV. Clinically, HCV can establish a persistent, chronic infection contributing to progressive liver disease, including cirrhosis and hepatocellular carcinoma (HCC), requiring intensive treatment regimens, possible liver transplantation and long-term care. Due to the chronic nature of HCV infection and the tremendous burden on healthcare resources, clinicians and laboratorians have looked for key epidemiological, pathological and viral characteristics that may provide insight into disease progression, severity and response to therapy to permit the administration of effective therapeutic regimens as well as long-term management of infected individuals. Determination of viral genotype has been identified as one parameter that could provide direction in the clinical management of patients with chronic HCV infections. The following review provides background on determination of HCV genotypes and the relevance of viral genome characterization in the current clinical setting.

/pdf/chronic-hepatitis-c-and-genotyping-the-clinical-significance-3n40xjlnte.pdf

Chronic Hepatitis C and Genotyping: The Clinical Significance of Determining HCV Genotypes:

The present investigation attempted to determine the exact prevalence of hepatitis D virus (HDV) infection among inhabitants of Miyako Island (a remote island in the Okinawa Prefecture) and the molecular characteristics of the HDV genome that was isolated. Among the 4728 inhabitants, 375 (7.9%) were hepatitis B surface antigen (HBsAg) positive. Antibody to HDV (anti-HDV) was present in 32 (8. 5%) of these 375 subjects, and liver function tests were normal in most subjects. The presence of HDV RNA was analysed by nested polymerase chain reaction (PCR). Thirteen out of the 32 anti-HDV antibody-positive subjects were HDV RNA positive. Thus, 3.5% of HBsAg-positive subjects on Miyako Island were HDV RNA positive. Among the HDV RNA-positive subjects, liver function tests were within normal limits or were mildly abnormal. Nucleotide sequence analysis revealed that the HDV genomes on Miyako Island were similar to the Japanese and Taiwan isolates of HDV genotype II. Taiwan is geographically close to Miyako Island. Even though the races are different, a geographical factor was revealed to be significant with regard to HDV infection, which was spread in a closed environment.

Molecular analysis of hepatitis d virus infection in miyako island, a small japanese island

It is still unclear whether hepatitis G virus (HGV) and hepatitis C virus (HCV) co-infection influences the natural course of chronic HCV infection and the response to interferon (IFN) therapy. In this study, we investigated the HGV RNA changes and responses to IFN therapy of HGV RNA-positive hepatitis C patients. The presence of HGV RNA in 264 patients who received IFN therapy at our institute was examined using the nested reverse transcription-polymerase chain reaction with primers deduced from the 5' non-coding region (5'-NCR) of the HGV. We also analysed the nucleotide sequences of the 5'-NCR and HGV before and after IFN therapy. Twelve (4.5%) of the 264 patients with chronic hepatitis C were HGV RNA positive. Of these 12 patients, full information was available in nine. Of those nine, seven became HGV RNA negative during IFN therapy but in six of the seven a relapse occurred. HCV RNA was not detected 1 year after IFN therapy in six patients. The serum alanine aminotransferase (ALT) levels of all the HCV RNA-negative patients post-treatment was within the normal range, irrespective of their HGV RNA status. Nucleotide sequences did not change after IFN therapy in any patient. Hence, we confirm that HGV is sensitive to IFN therapy but the liver damage caused by HGV infection is very mild or does not modify the liver function tests.

Biochemical and virological response to interferon therapy in patients with chronic hepatitis C, co-infected with hepatitis G virus.

Affiliations: Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, 208-0011, Japan. National Hospital Organization, Murayama Medical Center, Tokyo 208-0011, Japan. Department of Virology 1, National Institute of Infectious Diseases; Tokyo 162-8640, Japan. Research Center for Drug and Vaccine Development, National Institute of Infectious Diseases; Tokyo, 162-8640, Japan. Department of Veterinary Science, National Institute of Infectious Diseases; Tokyo, 162-8640, Japan. Department of Pathology, National Institute of Infectious Diseases; Tokyo, 162-8640, Japan. These authors contributed equally Lead Contact

Safety and immunogenicity of Pfizer/BioNTech SARS-CoV-2 mRNA third booster vaccine against SARS-CoV-2 Omicron variant in Japanese healthcare workers Authors:

Highlights A novel assay system for evaluation of Fc g R-effector function in cynomolgus macaque PBMCs Several different cell types bound to HA-expressing cells in the Fc g R-dependent manner IgGs elicited by ﬂu vaccination induced Fc g R-dependent classical monocytes binding This assay system could facilitate the development of a universal inﬂuenza vaccine SUMMARY Several cross-protective antibodies that recognize a broad range of inﬂuenza A virus (IAV) strains are known to have functions in virus elimination such as Fc g receptor (Fc g R)-effector function and neutralizing activity against the head region. Although few studies have used primary cells as effector cells, the Fc g R-effector function was evaluated after isolating each cell subset. Herein, we established an original assay system to evaluate puriﬁed FI6 IgG-mediated binding to hemagglutinin (HA)-expressing cells by ﬂow cytometry using peripheral blood mononuclear cells from cynomolgus macaques. In addition, we evaluated the Fc g R-effector function of IAV vaccine-induced anti-HA antibodies in cynomolgus macaques after administering the split vaccine. We found several cell types, mainly classical monocytes, bound to HA-expressing target cells in an Fc g R-dependent manner, that were dominant in the binding of the cell population. Thus, this assay system could facilitate the development of a universal inﬂuenza vaccine. administration. The results showed that the antibodies induced by the split vaccine mediate FcR-dependent target-effector binding, and the main subset of the bound cell is classical monocytes. This assay system will be helpful for the development of a universal inﬂuenza vaccine because it will allow us to examine in detail the Fc g R-effector function of individual cells induced by antibodies from passive immunization or vaccine administration in NHPs.

Assessment of Fc g receptor-dependent binding of inﬂuenza hemagglutinin vaccine-induced antibodies in a non-human primate model

Patients with chronic hepatitis C infection show a gradual progression of fibrosis to liver cirrhosis and hepatocellular carcinoma (HCC). We studied whether the progression of liver fibrosis differed among Japanese subjects who were infected with different hepatitis C virus (HCV) genotypes. In 527 patients we examined whether there was a relationship between gender, age, history of blood transfusion, interval between date of blood transfusion and date of liver biopsy or date of diagnosis of HCC, serum alanine aminotransferase level, platelet count or HCV genotype, with the extent of liver fibrosis, classified into four stages (F1–F4). Moreover, we compared the mean rate of liver fibrosis progression per year in patients with each HCV genotype. Patients who had a higher fibrosis score tended to be older, have a lower platelet count and a longer interval since blood transfusion than those who had a lower fibrosis score. The mean rate of liver fibrosis progression was 0.12 ± 0.15 stages per year after the blood transfusion. However, the progression rate of liver fibrosis in patients who had received a blood transfusion when they were ≥ 30 years of age was 0.19 ± 0.22, while the progression rate of liver fibrosis in the patients who had received a blood transfusion when they were < 30 years was 0.09 ± 0.09. In conclusion, chronic hepatitis C is a progressive disease, and patients with genotype 1b, 2a and 2b have a similar rate of progression of liver fibrosis. Particular attention should be paid to patients who are infected with HCV when ≥ 30 years of age, because intrahepatic fibrosis rapidly progresses in these patients.

Natural course of progression of liver fibrosis in Japanese patients with chronic liver disease type C--a study of 527 patients at one establishment.

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