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Host-Virus Interaction
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Host-Virus Interaction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 May 2026 | Viewed by 6288

Special Issue Editors

Dr. Xiaohui Ju

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Guest Editor
Fred Hutchinson Cancer Center, Seattle, WA 98109, USA
Interests: alphavirus; coronavirus; viral replication; virus-host interaction; viral evolution; deep mutational scanning
Dr. Xupeng Hong

E-Mail
Guest Editor
Laboratory of Virology and Infectious Disease, Science for Benefit of the Humanity, Rockefeller University, New York, NY 10065, USA
Interests: hepatitis B virus; virus disease; molecular virology

Special Issue Information

Dear Colleagues,

Viral infectious diseases continue to pose grave risks to public health. To better respond to emerging and re-emerging viruses, it is crucial to develop a comprehensive understanding of viral life cycles and virus–host interactions. Viruses rely on hijacking host cellular machinery for entry, replication, and propagation, while a host employs diverse defense strategies, including interferon signaling, autophagy, RNA interference, and the deployment of restriction factors to counteract infection. However, viruses have developed evasion strategies, such as escaping recognition from intracellular sensors, inhibiting interferon signaling pathways, manipulating host gene expression, and regulating the autophagy and degradation pathways. This ongoing molecular arms race between viruses and host cells ultimately shapes the outcome of infections. These insights into virus–host interactions enhance our understanding of viral pathogenesis and are essential for the development of effective antiviral strategies, vaccines, and therapeutics.

In this Special Issue of the International Journal of Molecular Sciences, we invite all types of manuscripts, including reviews, research articles, and short communications, focusing on virus–host interactions. Through this collection of articles, we hope that we can advance our knowledge on virus–host interactions so that we have a faster and more effective pandemic response in the future.

This Special Issue is supervised by Dr. Xupeng Hong and Dr. Xiaohui Ju and assisted by our Guest Editor Assistant Dr. Yan Wang (, University of Texas Medical Branch).

Dr. Xiaohui Ju
Dr. Xupeng Hong
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 250 words) can be sent to the Editorial Office for assessment.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • viral entry
  • viral replication
  • virus assembly and release
  • pro-viral factors
  • restriction factors
  • interferon pathway
  • viral immune evasion
  • antiviral strategies

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Published Papers (4 papers)

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Research

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25 pages, 5724 KB  
Article
Phosphoproteome-Entailed Kinase–Substrate Landscape of Human–DENV-2 Interaction
by Ayisha A. Jabbar, Vineetha Shaji, Akash Anil, Mahammad Nisar, Sowmya Soman, Ganesh Prasad, Chandran S. Abhinand, Prashant Kumar Modi, Madathiparambil Gopalakrishnan Madanan, Abhithaj Jayanandan, Rajendra Pilankatta and Rajesh Raju
Int. J. Mol. Sci. 2026, 27(6), 2718; https://doi.org/10.3390/ijms27062718 - 17 Mar 2026
Viewed by 686
Abstract
Dengue virus (DENV) is a mosquito-borne RNA virus that causes serious illness in humans, ranging from mild fever to severe clinical manifestations, with dengue virus type 2 (DENV-2) being the most virulent among its four serotypes. Despite extensive research, no specific antiviral therapy [...] Read more.
Dengue virus (DENV) is a mosquito-borne RNA virus that causes serious illness in humans, ranging from mild fever to severe clinical manifestations, with dengue virus type 2 (DENV-2) being the most virulent among its four serotypes. Despite extensive research, no specific antiviral therapy is currently available, making the host-directed method an appealing therapeutic approach. Evidence shows that DENV manipulates host kinase-driven phosphorylation pathways to control viral pathogenesis. Using the kinase–substrate phosphomotif approach, we predicted phosphorylation sites across the DENV proteome and their potential human kinases. The predicted kinase–substrate interactions were systematically integrated with DENV-2-induced human phosphoproteome datasets, protein–protein interactions, and experimentally-validated viral phosphosites. The therapeutic relevance of the identified host kinases was corroborated by the impact of their inhibitors on DENV-2 infection. Among the 359 potential human kinases predicted to phosphorylate DENV-2 proteins, based on human phosphoproteome and kinase–viral protein interaction analyses, CDK9 emerged as a central hub kinase. Molecular docking analyses further revealed that the host kinases CDK9, EEF2K, HASPIN, and TNNI3K form stable interactions with the viral capsid and NS5 proteins. Additionally, a conservation analysis suggested that the predicted phosphorylation sites are evolutionarily conserved across DENV-2 strains. Computational prediction tools supported the predicted kinase–substrate interactions, underscoring the role of host kinases as key regulators of DENV infection, which may act as potential therapeutic targets. This study highlights the interplay between dengue viral and host proteins, providing insights into host-directed therapeutic strategies for DENV-2 infection and their potential to address the current lack of effective antiviral interventions. Full article
(This article belongs to the Special Issue Host-Virus Interaction)
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15 pages, 19921 KB  
Article
Ultrastructural Insight into Rift Valley Fever Virus Pathogenesis in Different Human Cell Types
by Daniele Lapa, Maria Anele Romeo, Leonardo Duca, Carlotta Castelli, Eliana Specchiarello, Fabrizio Maggi and Laura Falasca
Int. J. Mol. Sci. 2025, 26(17), 8183; https://doi.org/10.3390/ijms26178183 - 23 Aug 2025
Viewed by 1478
Abstract
Rift Valley Fever Virus (RVFV) is an arbovirus that predominantly affects sheep, goats, and cattle, causing epizootics in livestock and epidemics in humans. Infection in pregnant livestock leads to high abortion rates and neonatal mortality. In humans, RVFV usually causes a self-limiting febrile [...] Read more.
Rift Valley Fever Virus (RVFV) is an arbovirus that predominantly affects sheep, goats, and cattle, causing epizootics in livestock and epidemics in humans. Infection in pregnant livestock leads to high abortion rates and neonatal mortality. In humans, RVFV usually causes a self-limiting febrile illness, but severe forms can develop, such as hepatitis, hemorrhage, encephalitis, and death. In addition, the association between RVFV infection during pregnancy and miscarriages or stillbirths has been documented. RVFV is transmitted by a range of mosquito species, and, due to the diffusion of these insects, the virus has spread in several world regions, making possible the risk of a public health emergency. Nevertheless, research remains limited and cellular pathology is still poorly characterized. This work aimed to fill some knowledge gaps on the comprehension of RVFV pathogenesis. For this purpose, transmission electron microscopy (TEM) was used to analyze cellular modifications associated with RVFV morphogenesis in four human cell lines (HuH-7, LAN-5, A549, and HTR-8/SVneo) derived from liver, brain, lung, and placenta. Our results showed that all four cell lines are permissive to RVFV infection and highlighted differences in the cytopathogenesis associated with the cell type. These findings could have important implications in understanding disease mechanisms and developing antiviral strategies. Full article
(This article belongs to the Special Issue Host-Virus Interaction)
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Review

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22 pages, 3813 KB  
Review
Host Responses to SARS-CoV-2 with an Emphasis on Cytokines
by Hideki Hayashi, Yoshinao Kubo and Yoshimasa Tanaka
Int. J. Mol. Sci. 2026, 27(2), 664; https://doi.org/10.3390/ijms27020664 - 9 Jan 2026
Viewed by 975
Abstract
The COVID-19 pandemic has profoundly affected societies around the world. Although the emergency phase of coronavirus disease 2019 (COVID-19) has ended, the threat it poses remains persistent. This review aims to clarify the mechanisms of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection [...] Read more.
The COVID-19 pandemic has profoundly affected societies around the world. Although the emergency phase of coronavirus disease 2019 (COVID-19) has ended, the threat it poses remains persistent. This review aims to clarify the mechanisms of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection to support effective management of the disease. A central focus is the host cellular response to the viral infection, with particular emphasis on the role of cytokines. Cytokines play a dual role in antiviral defense: they contribute to the inhibition of viral replication and facilitate the clearance of pathogens, yet dysregulated cytokine responses can result in severe immunopathology. Interferons (type I, type II, and type III) and other cytokines are pivotal in activating intracellular antiviral mechanisms and in orchestrating the recruitment of immune cells through extracellular signaling. Effective immune responses to viral infections are governed not only by primary immune cells—such as dendritic cells, T lymphocytes, and B lymphocytes—but also by the local cytokine milieu shaped by infected and neighboring cells. Given the presence of endogenous inhibitors and autoantibodies in vivo, it is essential to evaluate the functional activity of cytokines in clinical samples. We propose a novel approach to quantify biologically active cytokine levels. Full article
(This article belongs to the Special Issue Host-Virus Interaction)
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18 pages, 941 KB  
Review
Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection
by Qian Wang, Xing Wu, Mingchen Liu, Lu Li, Ying Wang, Qian He, Xuanxuan Zhang, Zhenglun Liang, Fan Gao and Xiao Ma
Int. J. Mol. Sci. 2025, 26(16), 7992; https://doi.org/10.3390/ijms26167992 - 19 Aug 2025
Cited by 2 | Viewed by 2402
Abstract
Enterovirus A71 (EVA71) is a major pathogen that causes hand, foot, and mouth disease (HFMD). Although the symptoms of HFMD can be self-limiting, severe meningitis, encephalitis, myocarditis, and acute flaccid paralysis may occur. Upon EVA71 infection, the host cells deploy an intricate network [...] Read more.
Enterovirus A71 (EVA71) is a major pathogen that causes hand, foot, and mouth disease (HFMD). Although the symptoms of HFMD can be self-limiting, severe meningitis, encephalitis, myocarditis, and acute flaccid paralysis may occur. Upon EVA71 infection, the host cells deploy an intricate network of factors to orchestrate cellular responses and maintain cellular homeostasis. However, the virus has evolved various strategies to avoid unfavorable host restrictions and to establish a productive infection process. As response regimens are correlated with disease symptoms, exploring the interactions between the virus and host contributes to understanding the pathogenesis and underlying mechanisms of infection. In this review, we summarized the recent research progress related to pro-viral factors during EVA71 infection and discussed the underlying mechanisms employed by EVA71 to facilitate virion production. These insights may help identify antiviral therapeutic candidates and support vaccine development. Full article
(This article belongs to the Special Issue Host-Virus Interaction)
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