Molecular Epidemiology in Hepatitis C Virus (HCV) Infection: Studies of Viral and Human Genomes

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Gastroenterology & Hepatopancreatobiliary Medicine".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 6800

Special Issue Editors


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Guest Editor
Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Madrid, Spain
Interests: HIV; hepatitis C; infectious diseases; immunology; virology; genetics; epidemiology; cirrhosis
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Guest Editor
Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain
Interests: hepatitis C; molecular virology; innate immunity; virus-host interaction; antibody; inflammation; immunopathology; vaccine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hepatitis C virus (HCV) is a major health problem, causing chronic hepatitis C to 71 million people, who are at risk for serious liver diseases. The recently used direct-acting antivirals (DAAs) eliminate HCV infection in more than 95% of patients, raising the possibility of controlling, and even eradicating, HCV infection.

Molecular epidemiology in HCV infection has mainly focused on studying the viral genetic diversity, but the host genetic background plays a major role in the spontaneous elimination of HCV infection and in the progression of chronic hepatitis C. Deep sequencing technology, in which virus variants infecting one individual can be distinguished and quantitated, has led to major advances in viral epidemiology. This has given rise to new challenges in the study of HCV molecular epidemiology, such as the selection of viral variants harboring resistance-associated substitutions (RAS) linked to DAA failure, and the characteristics of viruses in patients screened for HCV infection. Moreover, sequencing techniques and genotyping technologies can also be applied to host genomes, which play a major role in the spontaneous elimination of HCV infection and in the progression of chronic hepatitis C.

For this Special Issue, we invite you to submit studies focused on the HCV molecular epidemiology, from the virus and host perspectives, that can help to manage HCV infection in the DAAs era.

Dr. Salvador Resino
Dr. Isidoro Martínez
Guest Editors

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Keywords

  • hepatitis C
  • acute hepatitis
  • chronic hepatitis
  • HCV reinfection
  • HCV screening
  • HCV genotypes
  • HCV resistance-associated substitutions (RAS)
  • single nucleotide polymorphisms (SNPs)
  • HCV spontaneous clearance
  • liver disease progression

Published Papers (3 papers)

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Editorial

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4 pages, 212 KiB  
Editorial
The Challenging Road to Hepatitis C Virus Eradication
by Isidoro Martínez, Pablo Ryan, Jorge Valencia and Salvador Resino
J. Clin. Med. 2021, 10(4), 611; https://doi.org/10.3390/jcm10040611 - 5 Feb 2021
Cited by 6 | Viewed by 2071
Abstract
Hepatitis C virus (HCV) infection remains a substantial health problem as a leading cause of chronic liver disease worldwide [...] Full article

Research

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18 pages, 4616 KiB  
Article
Dissimilar Conservation Pattern in Hepatitis C Virus Mutant Spectra, Consensus Sequences, and Data Banks
by Carlos García-Crespo, María Eugenia Soria, Isabel Gallego, Ana Isabel de Ávila, Brenda Martínez-González, Lucía Vázquez-Sirvent, Jordi Gómez, Carlos Briones, Josep Gregori, Josep Quer, Celia Perales and Esteban Domingo
J. Clin. Med. 2020, 9(11), 3450; https://doi.org/10.3390/jcm9113450 - 27 Oct 2020
Cited by 10 | Viewed by 2071
Abstract
The influence of quasispecies dynamics on long-term virus diversification in nature is a largely unexplored question. Specifically, whether intra-host nucleotide and amino acid variation in quasispecies fit the variation observed in consensus sequences or data bank alignments is unknown. Genome conservation and dynamics [...] Read more.
The influence of quasispecies dynamics on long-term virus diversification in nature is a largely unexplored question. Specifically, whether intra-host nucleotide and amino acid variation in quasispecies fit the variation observed in consensus sequences or data bank alignments is unknown. Genome conservation and dynamics simulations are used for the computational design of universal vaccines, therapeutic antibodies and pan-genomic antiviral agents. The expectation is that selection of escape mutants will be limited when mutations at conserved residues are required. This strategy assumes long-term (epidemiologically relevant) conservation but, critically, does not consider short-term (quasispecies-dictated) residue conservation. We calculated mutant frequencies of individual loci from mutant spectra of hepatitis C virus (HCV) populations passaged in cell culture and from infected patients. Nucleotide or amino acid conservation in consensus sequences of the same populations, or in the Los Alamos HCV data bank did not match residue conservation in mutant spectra. The results relativize the concept of sequence conservation in viral genetics and suggest that residue invariance in data banks is an insufficient basis for the design of universal viral ligands for clinical purposes. Our calculations suggest relaxed mutational restrictions during quasispecies dynamics, which may contribute to higher calculated short-term than long-term viral evolutionary rates. Full article
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Other

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10 pages, 571 KiB  
Brief Report
TRPM5 rs886277 Polymorphism Predicts Hepatic Fibrosis Progression in Non-Cirrhotic HCV-Infected Patients
by Salvador Resino, Amanda Fernández-Rodríguez, Daniel Pineda-Tenor, Ana Zaida Gómez-Moreno, Juan José Sánchez-Ruano, Tomas Artaza-Varasa, María José Muñoz-Gómez, Ana Virseda-Berdices, María Martín-Vicente, Isidoro Martínez and María A. Jiménez-Sousa
J. Clin. Med. 2021, 10(3), 483; https://doi.org/10.3390/jcm10030483 - 28 Jan 2021
Cited by 1 | Viewed by 1949
Abstract
Background: TRPM5 (transient receptor potential cation channel subfamily M member 5) rs886277 polymorphism has been related to liver cirrhosis from different etiologies. The present study investigates the association of TRPM5 rs886277 polymorphism with liver fibrosis progression and cirrhosis development in chronic hepatitis C [...] Read more.
Background: TRPM5 (transient receptor potential cation channel subfamily M member 5) rs886277 polymorphism has been related to liver cirrhosis from different etiologies. The present study investigates the association of TRPM5 rs886277 polymorphism with liver fibrosis progression and cirrhosis development in chronic hepatitis C (CHC) patients. Methods: We conducted a retrospective study of 208 non-cirrhotic patients with CHC, who had at least two liver stiffness measurements (LSM) with a separation of 12 months (baseline LSM (LSM1) and the last LSM (LSM2)). Two outcome variables were considered: (1) LSM2/LSM1 ratio; (2) cirrhosis progression (F4; LSM ≥ 12.5 kPa). DNA genotyping was done at the CeGen using a MassARRAY platform. Results: The follow-up time was similar irrespective of the rs886277 genotype (46.4 months in TT genotype, 46.4 months in CT genotype, and 49.2 months in CC genotype; p = 0.649). The highest LSM increases were found in patients with CC genotype compared with TT and CT genotypes (p = 0.044 and p = 0.038, respectively). The cirrhosis progression was higher in patients with CC genotype than TT genotype (p = 0.033). Thus, the rs886277 C allele was associated with higher cirrhosis progression (adjusted odds ratio (aOR) = 2.64; p = 0.014). Moreover, rs886277 CC genotype was also related to higher values of LSM2/LSM1 ratio (adjusted arithmetic mean ratio a(AMR) = 1.31; p = 0.001) and cirrhosis progression (aOR = 4.33; p = 0.027). Conclusions: TRPM5 rs886277 polymorphism was associated with liver fibrosis progression and cirrhosis development among hepatitis C virus (HCV)-infected patients. Specifically, the rs886277 C allele and CC genotype were risk factors for advancing liver fibrosis and cirrhosis compared to the rs886277 T allele and CT/TT genotype, respectively. Full article
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