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Order Amarillovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The Amarillovirales order currently involves one family, namely Flaviviridae, 4 genera, and 89 species. The genera are Flavivirus, Hepacivirus, Pegivirus, and Pestivirus. Most infect mammals and birds. Many of them are host-specific and highly pathogenic, such as hepatitis C virus (HCV) of the genus Hepacivirus. After HCV, a major human pathogen-causing progressive liver disease (Yu ML and Chuang 2021), the Hepacivirus genus involves several other viruses of unknown pathogenicity that infect horses, rodents, bats, cows, and primates (Scheel et al. 2015).
Cancer-Causing Viruses
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Satya P. Gupta, Vertika Gautam
HCV is a single-stranded RNA virus of the Hepacivirus genus in the Flaviviridae family. It is the only positive-stranded RNA virus among the human oncogenic viruses. The length of the HCV genome is approximately 9.6 kb with a polyprotein of about 3,000 amino acids encoded in it. This polyprotein precursor is cleaved by cellular and viral proteases into three structural proteins (core, E1, E2) and seven nonstructural proteins (p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B) (Lindenbach and Rice 2005). Both envelope proteins (E1 and E2) are highly glycosylated and important in cell entry. E1 serves as the fusogenic subunit, and E2 acts as the receptor-binding protein. Of the nonstructural proteins, the NS5B protein (65 kDa) is the viral RNA-dependent RNA polymerase, which has the key function of replicating the HCV’s viral RNA by using the viral positive RNA strand as its template. NS5B catalyzes the polymerization of ribonucleoside triphosphates (rNTP) during RNA replication (Moradpour et al. 2007; Rigat et al. 2010).
Viral Hepatitis
Published in Thomas T. Yoshikawa, Shobita Rajagopalan, Antibiotic Therapy for Geriatric Patients, 2005
Abbasi J. Akhtar, Made Sutjita
HCV is an RNA virus belonging to Hepacivirus genus of the Flaviviridae family. HCV genotypes la and lb account for 75% of HCV infections in the United States. More genotypes and quasispecies are being recognized (35). The exact role of ethnicity in the prevalence of disease progression of HCV is unclear but appears to be substantial. Serum iron, ALT levels, histological disease activity index, and response to treatment were significantly lower in African-American as compared with Caucasian patients (36). In the United States HCV-associated cirrhosis is an important cause of hepatocellular carcinoma and is the most common reason for liver transplantation; HCV accounts for approximately 12,000 deaths every year. Approximately three-fourths of infected persons will develop chronic infection with approximately one-quarter going on to cirrhosis. As the population ages, it is anticipated that there will be an increasing number of individuals with chronic hepatitis C infection.
The next generation of HCV vaccines: a focus on novel adjuvant development
Published in Expert Review of Vaccines, 2021
Kimia Kardani, Seyed Mehdi Sadat, Mona Kardani, Azam Bolhassani
In the 1970s, most blood transfusion infections were linked to either hepatitis A or B virus. Primarily known as ‘non-A, non-B’ hepatitis, HCV was first recognized after discovery of its genome in 1989 [17]. The virus is a member of the Hepacivirus genus and Flaviviridae family that possesses an envelope and positive-sense single stranded ribonucleic acid (RNA) genome (9.6 kb). Figure 1 illustrates the structure of HCV. The genome of HCV is translated into a single large polyprotein containing approximately 3,000 amino acids, which is processed into 10 mature viral proteins by viral and cellular proteases. These viral proteins are divided into three structural proteins (core, E1, E2) and seven non-structural (NS) proteins (p7, NS2, NS3, NS4A, NS4B, NS5A, NS5B) [2]. The genome organization of HCV is shown in Figure 2. There are eight major HCV genotypes [18], and genotype 1 is the most prevalent, followed by genotypes 3, 4 and 2. There is about 30% genetic diversity among various HCV genotypes [18,19]. Moreover, HCV is called lipo-viro particles due to a fusion between cellular and viral components. Cellular proteins involved in the lipo-viro particles are apolipoproteins (Apo) A-I, Apo B, APO c-II, and Apo E [20–22].
Prevalence, risk factors and impact of occult HCV infection on liver morbidity among haemodialysis patients: hospital-based cross-sectional study
Published in Scandinavian Journal of Gastroenterology, 2020
Abdulrahman Alduraywish, Mostafa Ragheb, Ibrahim Taher, Nageh Louis, Khaled Aldossari, Rania Kishk
Infection with the hepatitis C virus (HCV) is a worldwide health problem that affects 2.5% of the population [1]. The virus belongs to the family of Flaviviridae and genus Hepacivirus [2]. Diagnosis of HCV infection is made by assessment of risk factors, clinical manifestations, abnormal liver enzymes and anti-HCV (HCV Ab) seroreactivity [3]. This common asymptomatic infection mostly turns chronic and diagnosis is made accidentally during routine testing. Although acute hepatitis is uncommonly encountered, HCV infection is related to variable liver morbidities that range from chronic hepatitis, cirrhosis and hepatocellular carcinoma [4,5]. Treatment of HCV depends largely on the presence of HCV RNA viraemia and more recently the direct-acting antiviral (DAA) that eliminated the virus in more than 90% of naïve cases [6,7].
Serum biomarkers for diagnosis and monitoring viral hepatitis and hepatocellular carcinoma
Published in Expert Review of Molecular Diagnostics, 2018
Sreelakshmi Kotha, ShuetFong Neong, Keyur Patel
HCV was discovered in 1989 from a cDNA clone derived from blood borne non-A, non-B viral hepatitis genome sequences [58]. HCV is an enveloped positive-sense virus classified in the Hepacivirus genus within the Flaviviridae family. Acute HCV is usually asymptomatic, and spontaneous resolution may occur in 15–45% in the first six months following exposure [59]. Most patients develop chronic infection following exposure, and retrospective analyses of posttransfusion hepatitis suggest that 75–85% of patients with acute infection develop chronic disease with risk of progression to cirrhosis [60]. HCV remains a leading cause of end-stage liver disease and liver transplantation worldwide [61–66]. The global prevalence of chronic HCV (CHC) infection was previously estimated at 2.35% or ~ 160 million individuals [67,68], but with newer and effective oral antiviral therapy the global prevalence has fallen significantly to 71.1 million [69]. Several studies identify the development of cirrhosis in 20% of CHC patients, whilst HCC occurred in 1–5%, around two decades after onset of infection [61]. Most patients remain undiagnosed, and this has implications on global health due to shared risk behaviors and unavailability of vaccines for prophylaxis. However, the dramatic development in therapeutics for HCV over the last decade has resulted in several available all oral direct-acting antiviral agents (DAA), with a high probability of achieving cure and potential eradication amongst low-risk populations, with sustained virologic response rates of most regimens now approaching 95–99%.