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Molecular Biology of Viral Replication and Associated Disease Outcomes
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Molecular Biology of Viral Replication and Associated Disease Outcomes

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 21 May 2025 | Viewed by 3592

Special Issue Editor

Dr. Usama Ashraf

E-Mail Website
Guest Editor
Institute for Immunity, Transplantation, and Infection, Stanford University, Stanford, CA, USA
Interests: molecular virology; host–virus interaction; viral pathogenesis; viral innate immunology; antivirals; RNA biology; serology of viral infections; virus evolution

Special Issue Information

Dear Colleagues,

I am pleased to invite you to submit articles on molecular insights into viral replication and associated disease outcomes. Viral replication involves a series of intricate steps, beginning with the virus attaching to and entering the host cell, then uncoating its genome, replicating and transcribing its genetic material, synthesizing viral proteins, assembling new virions, and finally releasing these virions to infect new cells. During replication, viruses exhibit diverse strategies depending on their type, such as DNA viruses using a host's nuclear machinery and RNA viruses, frequently relying on specialized viral enzymes like RNA-dependent RNA polymerase. In response to viral replication, disease outcomes vary widely and can range from acute, self-limiting illnesses to chronic and persistent infections. The host immune response plays a decisive role during infections, where innate immunity provides immediate, non-specific defense, whereas adaptive immunity offers a defined, long-term protective response. Understanding these processes is essential for establishing effective vaccines, antiviral therapies, and public health strategies to mitigate the burden of viral diseases in humans and animals.

In this Special Issue, original articles and reviews are welcome. Research may include, but is not limited to, the following:

  1. Mechanisms of viral ingress and egress from host cells.
  2. Mechanisms of viral replication (the transcription and translation of viral genes).
  3. Immunity to viral infections.
  4. Mechanisms of virus-mediated disease pathogenesis and disease outcomes.
  5. Therapeutic interventions to inhibit virus replication and mitigate disease outcomes.

I look forward to receiving your contributions.

Dr. Usama Ashraf
Guest Editor

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. Current Issues in Molecular Biology 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 2200 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

  • viruses
  • replication
  • immunity
  • pathogenesis
  • antivirals
  • immune modulator

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Published Papers (4 papers)

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Research

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15 pages, 4721 KiB  
Article
A Multi-Model Machine Learning Framework for Identifying Raloxifene as a Novel RNA Polymerase Inhibitor from FDA-Approved Drugs
by Nhung Thi Hong Van and Minh Tuan Nguyen
Curr. Issues Mol. Biol. 2025, 47(5), 315; https://doi.org/10.3390/cimb47050315 - 28 Apr 2025
Viewed by 117
Abstract
RNA-dependent RNA polymerase (RdRP) represents a critical target for antiviral drug development. We developed a multi-model machine learning framework combining five traditional algorithms (ExtraTreesClassifier, RandomForestClassifier, LGBMClassifier, BernoulliNB, and BaggingClassifier) with a CNN deep learning model to identify potential RdRP inhibitors among FDA-approved drugs. [...] Read more.
RNA-dependent RNA polymerase (RdRP) represents a critical target for antiviral drug development. We developed a multi-model machine learning framework combining five traditional algorithms (ExtraTreesClassifier, RandomForestClassifier, LGBMClassifier, BernoulliNB, and BaggingClassifier) with a CNN deep learning model to identify potential RdRP inhibitors among FDA-approved drugs. Using the PubChem dataset AID 588519, our ensemble models achieved the highest performance with accuracy, ROC-AUC, and F1 scores higher than 0.70, while the CNN model demonstrated complementary predictive value with a specificity of 0.77 on external validation. Molecular docking studies with the norovirus RdRP (PDB: 4NRT) identified raloxifene as a promising candidate, with a binding affinity (−8.8 kcal/mol) comparable to the positive control (−9.2 kcal/mol). The molecular dynamics simulation confirmed stable binding with RMSD values of 0.12–0.15 nm for the protein–ligand complex and consistent hydrogen bonding patterns. Our findings suggest that raloxifene may possess RdRP inhibitory activity, providing a foundation for its experimental validation as a potential broad-spectrum antiviral agent. Full article
(This article belongs to the Special Issue Molecular Biology of Viral Replication and Associated Disease Outcomes)
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15 pages, 508 KiB  
Article
HLA Class I (A and B) Allele Polymorphism in a Moroccan Population Infected with Hepatitis C Virus
by Safa Machraoui, Abdelmalek Hakmaoui, Khaoula Errafii, Mehdi Knidiri, Lamiaa Essaadouni, Khadija Krati and Brahim Admou
Curr. Issues Mol. Biol. 2024, 46(12), 14080-14094; https://doi.org/10.3390/cimb46120842 - 13 Dec 2024
Viewed by 1254
Abstract
Hepatitis C virus (HCV) infection is one of the major health burdens worldwide. Its course depends on the virus itself and the host’s immune responses. The latter are conditioned by immunogenetic factors, in particular human leukocyte antigens (HLAs), whose role in determining the [...] Read more.
Hepatitis C virus (HCV) infection is one of the major health burdens worldwide. Its course depends on the virus itself and the host’s immune responses. The latter are conditioned by immunogenetic factors, in particular human leukocyte antigens (HLAs), whose role in determining the outcome of infection varies according to populations and ethnic groups. The current study attempted to investigate the possible relationship between HLA-A and HLA-B allele polymorphism and its impacts on the clinical outcome of HCV for a better understanding of disease susceptibility and clearance. A cross-sectional and comparative study was carried out on 40 patients with hepatitis C and 100 ethnically matched healthy control subjects originating from southern Morocco. HLA class I alleles were typed using the high-resolution PCR-SSO method. The prevalence of certain HLA class I alleles differed significantly between HCV-infected individuals and healthy controls. In particular, HLA-A*02:01 was less prevalent in chronic HCV infection (p = 0.002), indicating a potential protective effect, while the higher prevalence of HLA-A*68:02, A*66:01 B*15:03, B*41:02, B*44:03, and B*50:01 in patients could indicate a predisposing factor. These findings support the association of these immunogenetic markers with HCV infection, indicating their possible role in determining clinical and genotype forms as well as the outcome of HCV infection. Thus, an in-depth analysis of these alleles could lead to a better understanding of HCV pathogenesis and potential targeted interventions. Full article
(This article belongs to the Special Issue Molecular Biology of Viral Replication and Associated Disease Outcomes)
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24 pages, 10905 KiB  
Article
Benchmark Investigation of SARS-CoV-2 Mutants’ Immune Escape with 2B04 Murine Antibody: A Step Towards Unraveling a Larger Picture
by Karina Kapusta, Allyson McGowan, Santanu Banerjee, Jing Wang, Wojciech Kolodziejczyk and Jerzy Leszczynski
Curr. Issues Mol. Biol. 2024, 46(11), 12550-12573; https://doi.org/10.3390/cimb46110745 - 6 Nov 2024
Cited by 1 | Viewed by 1413
Abstract
Even though COVID-19 is no longer the primary focus of the global scientific community, its high mutation rate (nearly 30 substitutions per year) poses a threat of a potential comeback. Effective vaccines have been developed and administered to the population, ending the pandemic. [...] Read more.
Even though COVID-19 is no longer the primary focus of the global scientific community, its high mutation rate (nearly 30 substitutions per year) poses a threat of a potential comeback. Effective vaccines have been developed and administered to the population, ending the pandemic. Nonetheless, reinfection by newly emerging subvariants, particularly the latest JN.1 strain, remains common. The rapid mutation of this virus demands a fast response from the scientific community in case of an emergency. While the immune escape of earlier variants was extensively investigated, one still needs a comprehensive understanding of how specific mutations, especially in the newest subvariants, influence the antigenic escape of the pathogen. Here, we tested comprehensive in silico approaches to identify methods for fast and accurate prediction of antibody neutralization by various mutants. As a benchmark, we modeled the complexes of the murine antibody 2B04, which neutralizes infection by preventing the SARS-CoV-2 spike glycoprotein’s association with angiotensin-converting enzyme (ACE2). Complexes with the wild-type, B.1.1.7 Alpha, and B.1.427/429 Epsilon SARS-CoV-2 variants were used as positive controls, while complexes with the B.1.351 Beta, P.1 Gamma, B.1.617.2 Delta, B.1.617.1 Kappa, BA.1 Omicron, and the newest JN.1 Omicron variants were used as decoys. Three essentially different algorithms were employed: forced placement based on a template, followed by two steps of extended molecular dynamics simulations; protein–protein docking utilizing PIPER (an FFT-based method extended for use with pairwise interaction potentials); and the AlphaFold 3.0 model for complex structure prediction. Homology modeling was used to assess the 3D structure of the newly emerged JN.1 Omicron subvariant, whose crystallographic structure is not yet available in the Protein Database. After a careful comparison of these three approaches, we were able to identify the pros and cons of each method. Protein–protein docking yielded two false-positive results, while manual placement reinforced by molecular dynamics produced one false positive and one false negative. In contrast, AlphaFold resulted in only one doubtful result and a higher overall accuracy-to-time ratio. The reasons for inaccuracies and potential pitfalls of various approaches are carefully explained. In addition to a comparative analysis of methods, some mechanisms of immune escape are elucidated herein. This provides a critical foundation for improving the predictive accuracy of vaccine efficacy against new viral subvariants, introducing accurate methodologies, and pinpointing potential challenges. Full article
(This article belongs to the Special Issue Molecular Biology of Viral Replication and Associated Disease Outcomes)
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Review

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10 pages, 406 KiB  
Review
The MAPK Response to Virus Infection Is Modified by Probenecid
by Les P. Jones, David E. Martin and Ralph A. Tripp
Curr. Issues Mol. Biol. 2025, 47(4), 246; https://doi.org/10.3390/cimb47040246 - 2 Apr 2025
Viewed by 272
Abstract
Respiratory viruses such as respiratory syncytial virus (RSV) annually cause respiratory illness, which may result in substantial disease and mortality in susceptible individuals. Viruses exploit host cell machinery for replication, which engages the mitogen-activated protein kinases (MAPK) pathway. The MAPK signaling pathways are [...] Read more.
Respiratory viruses such as respiratory syncytial virus (RSV) annually cause respiratory illness, which may result in substantial disease and mortality in susceptible individuals. Viruses exploit host cell machinery for replication, which engages the mitogen-activated protein kinases (MAPK) pathway. The MAPK signaling pathways are triggered by pattern recognition receptors that recognize the pathogen, infection, or external stimuli, leading to the induction and regulation of immunity and inflammation. Probenecid, used to improve renal function by inhibiting the tubular reabsorption of uric acid, has been shown to have therapeutic efficacy in reducing inflammation and blocking viral replication by inhibiting components of the MAPK pathway that preclude virus replication. This review summarizes key molecular cascades in the host response to virus recognition, infection, and replication and how this can be altered by probenecid treatment. Full article
(This article belongs to the Special Issue Molecular Biology of Viral Replication and Associated Disease Outcomes)
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