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Viruses
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Within-Host Viral Dynamics: A Window into Viral Evolution
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Within-Host Viral Dynamics: A Window into Viral Evolution

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 5127

Special Issue Editors

Dr. Xiaofeng Fan

E-Mail Website
Guest Editor
School of Medicine, St. Louis University, St. Louis, MO, USA
Interests: viral metagenomics; human genomics; bioinformatics; hepatitis viruses
Dr. Mahmoud Reza Pourkarim

E-Mail Website
Guest Editor
Laboratory for Clinical and Epidemiological Virology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, 3000 Leuven, Belgium
Interests: hepatitis B virus; blood virome; emerging infectious diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Evolution is the cornerstone in modern biomedicine. However, studying evolution is a challenge in higher organisms owing to their sizable genomes and low mutation rates. Measurable alterations related to evolution can take up to millions of years to develop. Given their tiny genomes, short replication cycles, and high mutation rates, viruses represent an attractive model for studying evolution in vivo. While the entire course of viral infection in hosts can be viewed as an evolutionary episode, our knowledge on underlying mechanisms that drive viral evolution is far from complete. How is the evolutionary process shaped by viral interaction with host innate and adaptive immunity? What is the contribution of the viral intrinsic mutation rate and replication strategy? Does the human microbiome influence viral evolution, and if so, how? Within-host viral dynamics provide an excellent opportunity to study these complex interactions and their roles in infection outcomes. The advent of deep sequencing techniques and other omics approaches now allow an unbiased investigation of the entire viral population in the context of micro- and macroenvironments. These articles will give us deep insights into viral evolution that are relevant to the prevention, diagnosis, and treatment of viral diseases.

Dr. Xiaofeng Fan
Dr. Mahmoud Reza Pourkarim
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • virome
  • metagenomics
  • phylogenetics
  • viral evolution
  • quasispecies
  • infectious diseases

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Published Papers (2 papers)

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26 pages, 7907 KiB  
Article
HPV, HBV, and HIV-1 Viral Integration Site Mapping: A Streamlined Workflow from NGS to Genomic Insights of Carcinogenesis
by Jane Shen-Gunther and Acarizia Easley
Viruses 2024, 16(6), 975; https://doi.org/10.3390/v16060975 - 18 Jun 2024
Viewed by 2645
Abstract
Viral integration within the host genome plays a pivotal role in carcinogenesis. Various disruptive mechanisms are involved, leading to genomic instability, mutations, and DNA damage. With next-generation sequencing (NGS), we can now precisely identify viral and host genomic breakpoints and chimeric sequences, which [...] Read more.
Viral integration within the host genome plays a pivotal role in carcinogenesis. Various disruptive mechanisms are involved, leading to genomic instability, mutations, and DNA damage. With next-generation sequencing (NGS), we can now precisely identify viral and host genomic breakpoints and chimeric sequences, which are useful for integration site analysis. In this study, we evaluated a commercial hybrid capture NGS panel specifically designed for detecting three key viruses: HPV, HBV, and HIV-1. We also tested workflows for Viral Hybrid Capture (VHC) and Viral Integration Site (VIS) analysis, leveraging customized viral databases in CLC Microbial Genomics. By analyzing sequenced data from virally infected cancer cell lines (including SiHa, HeLa, CaSki, C-33A, DoTc2, 2A3, SCC154 for HPV; 3B2, SNU-182 for HBV; and ACH-2 for HIV-1), we precisely pinpointed viral integration sites. The workflow also highlighted disrupted and neighboring human genes that may play a crucial role in tumor development. Our results included informative virus–host read mappings, genomic breakpoints, and integration circular plots. These visual representations enhance our understanding of the integration process. In conclusion, our seamless end-to-end workflow bridges the gap in understanding viral contributions to cancer development, paving the way for improved diagnostics and treatment strategies. Full article
(This article belongs to the Special Issue Within-Host Viral Dynamics: A Window into Viral Evolution)
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15 pages, 3386 KiB  
Article
Intra-Patient Genomic Variations of Human Papillomavirus Type 31 in Cervical Cancer and Precancer
by Gota Kogure, Kohsei Tanaka, Tomoya Matsui, Mamiko Onuki, Koji Matsumoto, Takashi Iwata and Iwao Kukimoto
Viruses 2023, 15(10), 2104; https://doi.org/10.3390/v15102104 - 17 Oct 2023
Cited by 1 | Viewed by 1855
Abstract
Human papillomavirus type 31 (HPV31) is detected less frequently in cervical cancer than two major causative types, HPV16 and HPV18. Here, we report a comprehensive analysis of HPV31 genome sequences in cervical lesions collected from Japanese women. Of 52 HPV31-positive cervical specimens analyzed [...] Read more.
Human papillomavirus type 31 (HPV31) is detected less frequently in cervical cancer than two major causative types, HPV16 and HPV18. Here, we report a comprehensive analysis of HPV31 genome sequences in cervical lesions collected from Japanese women. Of 52 HPV31-positive cervical specimens analyzed by deep sequencing, 43 samples yielded complete genome sequences of around 7900 base pairs and 9 samples yielded partially deleted genome sequences. Phylogenetic analysis showed that HPV31 variant distribution was lineage A in 19 samples (36.5%), lineage B in 28 samples (53.8%), and lineage C in 5 samples (9.6%), indicating that lineage B variants are dominant among HPV31 infections in Japan. Deletions in the viral genome were found in the region from the E1 to L1 genes, but all the deleted genomes retained the E6/E7 genes. Among intra-patient nucleotide variations relative to a consensus genome sequence in each sample, C-to-T substitutions were most frequently detected, followed by T-to-C and C-to-A substitutions. High-frequency, intra-patient mutations (>10%) in cervical cancer samples were found in the E1, E2, and E7 genes, and all of them were nonsynonymous substitutions. The enrichment of high-frequency nonsynonymous substitutions strongly suggests that these intra-patient mutations are positively selected during the development of cervical cancer/precancer. Full article
(This article belongs to the Special Issue Within-Host Viral Dynamics: A Window into Viral Evolution)
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