Special Issue "Viral Molecular Epidemiology"

A special issue of Viruses (ISSN 1999-4915).

Deadline for manuscript submissions: closed (31 July 2020).

Special Issue Editor

Dr. Allison Imrie
E-Mail Website
Guest Editor
Faculty of Health and Medical Sciences, Infection and Immunity, The University of Western Australia, Perth, Australia
Interests: Virus-specific cellular immunity; Molecular epidemiology; Immunogenetics; T cell receptor; Human immunodeficiency virus; Flaviviruses; Dengue

Special Issue Information

Dear Colleagues,

Viral molecular epidemiology coupled with phylogenetic analysis is a powerful approach for the investigation of transmission, diversity, and evolution and origin of viruses and to explore the determinants of disease transmission in human populations. Associations between viral genomes and disease pathogenesis and clinical outcomes may also be assessed. For example, analysis of human and animal coronavirus genomes identified in outbreaks and in surveillance programs since the emergence of SARS in 2002 has demonstrated the close relationship between human SARS CoV and bat CoV, indicating a bat origin for SARS CoV; similarly, the emergent novel coronavirus 2019-nCoV identified in patients with pneumonia of an unknown cause has been shown to be closely related yet distinct to SARS CoV, clustering with bat-derived SARS-like CoV. Incorporating molecular clock analysis to assess evolutionary origin and movement of viruses within and between countries informs our understanding of movement and dispersal of viruses and associations with disease severity, a recent example being Zika virus transmission in the Americas following likely introduction from French Polynesia. Molecular epidemiological studies using travelers as sentinels provide insights into virus transmission patterns in regions where viral genomic data are not widely reported and enhance our understanding of genome origin and evolution, and viral and epidemic virulence.

The purpose of this Special Issue is to present original research articles and reviews related to viral molecular epidemiology studies that describe transmission and evolution of human and animal viral pathogens.

Dr. Allison Imrie
Guest Editor

Manuscript Submission Information

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Keywords

  • virus genomics
  • virus evolution
  • molecular epidemiology
  • phylogeny
  • virus transmission
  • viral diversity
  • travelers

Published Papers (6 papers)

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Research

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Open AccessCommunication
Molecular Characterization of Dengue Type 2 Outbreak in Pacific Islands Countries and Territories, 2017–2020
Viruses 2020, 12(10), 1081; https://doi.org/10.3390/v12101081 - 25 Sep 2020
Cited by 1 | Viewed by 647
Abstract
Dengue virus (DENV) serotype-2 was detected in the South Pacific region in 2014 for the first time in 15 years. In 2016–2020, DENV-2 re-emerged in French Polynesia, Vanuatu, Wallis and Futuna, and New Caledonia, co-circulating with and later replacing DENV-1. In this context, [...] Read more.
Dengue virus (DENV) serotype-2 was detected in the South Pacific region in 2014 for the first time in 15 years. In 2016–2020, DENV-2 re-emerged in French Polynesia, Vanuatu, Wallis and Futuna, and New Caledonia, co-circulating with and later replacing DENV-1. In this context, epidemiological and molecular evolution data are paramount to decipher the diffusion route of this DENV-2 in the South Pacific region. In the current work, the E gene from 23 DENV-2 serum samples collected in Vanuatu, Fiji, Wallis and Futuna, and New Caledonia was sequenced. Both maximum likelihood and Bayesian phylogenetic analyses were performed. While all DENV-2 strains sequenced belong to the Cosmopolitan genotype, phylogenetic analysis suggests at least three different DENV-2 introductions in the South Pacific between 2017 and 2020. Strains retrieved in these Pacific Islands Countries and Territories (PICTs) in 2017–2020 are phylogenetically related, with strong phylogenetic links between strains retrieved from French PICTs. These phylogenetic data substantiate epidemiological data of the DENV-2 diffusion pattern between these countries. Full article
(This article belongs to the Special Issue Viral Molecular Epidemiology)
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Open AccessArticle
Molecular Characterization of Hemorrhagic Enteritis Virus (HEV) Obtained from Clinical Samples in Western Canada 2017–2018
Viruses 2020, 12(9), 941; https://doi.org/10.3390/v12090941 - 26 Aug 2020
Viewed by 679
Abstract
Hemorrhagic enteritis virus (HEV) is an immunosuppressive adenovirus that causes an acute clinical disease characterized by hemorrhagic gastroenteritis in 4-week-old turkeys and older. Recurrent incidence of secondary infections (e.g., systemic bacterial infections, cellulitis, and elevated mortality), may be associated with the presence of [...] Read more.
Hemorrhagic enteritis virus (HEV) is an immunosuppressive adenovirus that causes an acute clinical disease characterized by hemorrhagic gastroenteritis in 4-week-old turkeys and older. Recurrent incidence of secondary infections (e.g., systemic bacterial infections, cellulitis, and elevated mortality), may be associated with the presence of field-type HEV in Canadian turkey farms. We speculate that field-type HEV and vaccine/vaccine-like strains can be differentiated through analysis of the viral genomes, hexon genes, and the specific virulence factors (e.g., ORF1, E3, and fib knob domain). Nine out of sixteen spleens obtained from cases suspected of immunosuppression by HEV were analyzed. The limited data obtained showed that: (1) field-type HEV circulates in many non-vaccinated western Canadian flocks; (2) field-type HEV circulates in vaccinated flocks with increased recurrent bacterial infections; and (3) the existence of novel point mutations in hexon, ORF1, E3, and specially fib knob domains. This is the first publication showing the circulation of wild-type HEV in HEV-vaccinated flocks in Western Canada, and the usefulness of a novel procedure that allows whole genome sequencing of HEV directly from spleens, without passaging in cell culture or passaging in vivo. Further studies focusing more samples are required to confirm our observations and investigate possible vaccination failure. Full article
(This article belongs to the Special Issue Viral Molecular Epidemiology)
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Open AccessArticle
Dengue Virus Serotype 4 Is Responsible for the Outbreak of Dengue in East Java City of Jember, Indonesia
Viruses 2020, 12(9), 913; https://doi.org/10.3390/v12090913 - 20 Aug 2020
Viewed by 836
Abstract
Outbreaks of dengue virus (DENV) in Indonesia have been mainly caused by the DENV serotype-1; -2; or -3. The DENV-4 was the least-reported serotype in Indonesia during the last five decades. We recently conducted a molecular epidemiology study of dengue in the Jember [...] Read more.
Outbreaks of dengue virus (DENV) in Indonesia have been mainly caused by the DENV serotype-1; -2; or -3. The DENV-4 was the least-reported serotype in Indonesia during the last five decades. We recently conducted a molecular epidemiology study of dengue in the Jember regency, East Java province, Indonesia. Dengue is endemic in the region and outbreaks occur annually. We investigated the clinical characteristics and etiology of dengue-like febrile illness in this regency to understand the disease dynamics. A total of 191 patients with clinical symptoms similar to dengue were recruited during an 11-month study in 2019–2020. Children accounted for the majority of cases and dengue burden was estimated in 41.4% of the cases based on NS1 antigen, viral RNA, and IgG/IgM antibody detection with the majority (73.4%) being primary infections. Secondary infection was significantly associated with a higher risk of severe dengue manifestation. All four DENV serotypes were detected in Jember. Strikingly, we observed the predominance of DENV-4, followed by DENV-3, DENV-1, and DENV-2. Genotype determination using Envelope gene sequence revealed the classification into Genotype I, Cosmopolitan Genotype, Genotype I, and Genotype II for DENV-1, -2, -3, and -4, respectively. The predominance of DENV-4 in Jember may be associated with a new wave of DENV infections and spread in a non-immune population lacking a herd-immunity to this particular serotype. Full article
(This article belongs to the Special Issue Viral Molecular Epidemiology)
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Open AccessArticle
Next-Generation Sequencing-Based Quantitative Detection of Hepatitis B Virus Pre-S Mutants in Plasma Predicts Hepatocellular Carcinoma Recurrence
Viruses 2020, 12(8), 796; https://doi.org/10.3390/v12080796 - 24 Jul 2020
Cited by 8 | Viewed by 746
Abstract
Hepatocellular carcinoma (HCC) is among the most common and lethal human cancers worldwide. Despite curative resection, high recurrence of HCC remains a big threat, leading to poor patient outcomes. Hepatitis B virus (HBV) pre-S mutants, which harbor deletions over pre-S1 and pre-S2 gene [...] Read more.
Hepatocellular carcinoma (HCC) is among the most common and lethal human cancers worldwide. Despite curative resection, high recurrence of HCC remains a big threat, leading to poor patient outcomes. Hepatitis B virus (HBV) pre-S mutants, which harbor deletions over pre-S1 and pre-S2 gene segments of large surface proteins, have been implicated in HCC recurrence. Therefore, a reliable approach for detection of pre-S mutants is urgently needed for predicting HCC recurrence to improve patient survival. In this study, we used a next-generation sequencing (NGS)-based platform for quantitative detection of pre-S mutants in the plasma of HBV-related HCC patients and evaluated their prognostic values in HCC recurrence. We demonstrated that the presence of deletions spanning the pre-S2 gene segment and the high percentage of pre-S2 plus pre-S1 + pre-S2 deletions, either alone or in combination, was significantly and independently associated with poor recurrence-free survival and had greater prognostic performance than other clinicopathological and viral factors in predicting HCC recurrence. Our data suggest that the NGS-based quantitative detection of pre-S mutants in plasma represents a promising approach for identifying patients at high risk for HBV-related HCC recurrence after surgical resection in a noninvasive manner. Full article
(This article belongs to the Special Issue Viral Molecular Epidemiology)
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Open AccessArticle
Phylogenetic and Timescale Analysis of Barmah Forest Virus as Inferred from Genome Sequence Analysis
Viruses 2020, 12(7), 732; https://doi.org/10.3390/v12070732 - 06 Jul 2020
Cited by 2 | Viewed by 921
Abstract
Barmah Forest virus (BFV) is a medically important mosquito-borne alphavirus endemic to Australia. Symptomatic disease can be a major cause of morbidity, associated with fever, rash, and debilitating arthralgia. BFV disease is similar to that caused by Ross River virus (RRV), the other [...] Read more.
Barmah Forest virus (BFV) is a medically important mosquito-borne alphavirus endemic to Australia. Symptomatic disease can be a major cause of morbidity, associated with fever, rash, and debilitating arthralgia. BFV disease is similar to that caused by Ross River virus (RRV), the other major Australian alphavirus. Currently, just four BFV whole-genome sequences are available with no genome-scale phylogeny in existence to robustly characterise genetic diversity. Thirty novel genome sequences were derived for this study, for a final 34-taxon dataset sampled over a 44 year period. Three distinct BFV genotypes were characterised (G1–3) that have circulated in Australia and Papua New Guinea (PNG). Evidence of spatio-temporal co-circulation of G2 and G3 within regions of Australia was noted, including in the South West region of Western Australia (WA) during the first reported disease outbreaks in the state’s history. Compared with RRV, the BFV population appeared more stable with less frequent emergence of novel lineages. Preliminary in vitro assessment of RRV and BFV replication kinetics found that RRV replicates at a significantly faster rate and to a higher, more persistent titre compared with BFV, perhaps indicating mosquitoes may be infectious with RRV for longer than with BFV. This investigation resolved a greater diversity of BFV, and a greater understanding of the evolutionary dynamics and history was attained. Full article
(This article belongs to the Special Issue Viral Molecular Epidemiology)
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Review

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Open AccessReview
Hepatitis B Virus Pre-S Mutants as Biomarkers and Targets for the Development and Recurrence of Hepatocellular Carcinoma
Viruses 2020, 12(9), 945; https://doi.org/10.3390/v12090945 - 26 Aug 2020
Cited by 1 | Viewed by 1017
Abstract
Chronic hepatitis B virus (HBV) infection is a major risk factor for the development of hepatocellular carcinoma (HCC), the leading cause of cancer-related death worldwide. Despite progress in the prevention and therapy of HCC, high incidence and recurrence rates of HCC remain big [...] Read more.
Chronic hepatitis B virus (HBV) infection is a major risk factor for the development of hepatocellular carcinoma (HCC), the leading cause of cancer-related death worldwide. Despite progress in the prevention and therapy of HCC, high incidence and recurrence rates of HCC remain big threats, resulting in poor patient survival. Effective biomarkers and targets of HCC are therefore urgently needed for better management and to improve patient outcomes. Pre-S mutants have been well demonstrated as HBV oncoproteins that play important roles in HCC development through activation of multiple oncogenic signal pathways in hepatocytes, in vitro and in vivo. The presence of pre-S mutants in patients with chronic HBV infection and HBV-related HCC has been associated with a significantly higher risk of HCC development and recurrence after curative surgical resection, respectively. In this review, we summarize the roles of pre-S mutants as biomarkers for predicting HBV-related HCC development and recurrence, and highlight the pre-S mutants-activated oncogenic signal pathways as potential targets for preventing HBV-related HCC development. Full article
(This article belongs to the Special Issue Viral Molecular Epidemiology)
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