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Research on Virus-Induced Cellular and Molecular Responses
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Research on Virus-Induced Cellular and Molecular Responses

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: 31 December 2024 | Viewed by 3550

Special Issue Editor

Dr. Rudian Zhang

E-Mail Website
Guest Editor
Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75390, USA
Interests: autophagic degradation of protein aggregation; meiotic translational control; virology and insect immunity; virus infectivity

Special Issue Information

Dear Colleagues,

A virus is an intracellular parasite. Therefore, the initial stage of virus invasion is a battle between the virus and the cell it parasitizes. For multicellular organisms, in addition to the host’s immune mechanisms, cells themselves have developed some defense mechanisms against viral invasions, such as autophagy.

On the other hand, once the virus has invaded the cell, it will alter the internal environment of the cell through a series of cellular molecular responses to adapt to its survival and replication. However, these processes can trigger inflammation and even lead to significant cellular stress, ultimately resulting in cancer.

Therefore, the theme of this Special Issue helps us understand the mechanisms of how cells resist virial invasion, as well as the principles behind some carcinoma viruses. By welcoming original research and review articles on this theme, we are trying to integrate the current knowledge and help virologists, immunologists, and cellular molecular biologists to work together closely to address the viral diseases issues that have affected human beings for centuries.

We look forward to receiving your contributions.

Dr. Rudian Zhang
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

  • virus infectivity
  • infectious diseases
  • cellular stress
  • autophagy

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Published Papers (4 papers)

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Research

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16 pages, 3147 KiB  
Article
Comparison of the Proteome of Huh7 Cells Transfected with Hepatitis B Virus Subgenotype A1, with or without G1862T
by Kiyasha Padarath, Aurélie Deroubaix, Previn Naicker, Stoyan Stoychev and Anna Kramvis
Curr. Issues Mol. Biol. 2024, 46(7), 7032-7047; https://doi.org/10.3390/cimb46070419 - 4 Jul 2024
Viewed by 590
Abstract
HBeAg is a non-structural, secreted protein of hepatitis B virus (HBV). Its p25 precursor is post-translationally modified in the endoplasmic reticulum. The G1862T precore mutation leads to the accumulation of P25 in the endoplasmic reticulum and activation of unfolded protein response. Using mass [...] Read more.
HBeAg is a non-structural, secreted protein of hepatitis B virus (HBV). Its p25 precursor is post-translationally modified in the endoplasmic reticulum. The G1862T precore mutation leads to the accumulation of P25 in the endoplasmic reticulum and activation of unfolded protein response. Using mass spectrometry, comparative proteome profiling of Huh-7 cells transfected with wildtype (WT) or G1862T revealed significantly differentially expressed proteins resulting in 12 dysregulated pathways unique to WT-transfected cells and 7 shared between cells transfected with either WT or G1862T. Except for the p38 MAPK signalling pathway, WT showed a higher number of DEPs than G1862T-transfected cells in all remaining six shared pathways. Two signalling pathways: oxidative stress and cell cycle signalling were differentially expressed only in cells transfected with G1862T. Fifteen pathways were dysregulated in G1862T-transfected cells compared to WT. The 15 dysregulated pathways were involved in the following processes: MAPK signalling, DNA synthesis and methylation, and extracellular matrix organization. Moreover, proteins involved in DNA synthesis signalling (replication protein A (RPA) and DNA primase (PRIM2)) were significantly upregulated in G1862T compared to WT. This upregulation was confirmed by mRNA quantification of both genes and immunofluorescent confocal microscopy for RPA only. The dysregulation of the pathways involved in these processes may lead to immune evasion, persistence, and uncontrolled proliferation, which are hallmarks of cancer. Full article
(This article belongs to the Special Issue Research on Virus-Induced Cellular and Molecular Responses)
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Review

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13 pages, 1154 KiB  
Review
Targeting Cancers with oHSV-Based Oncolytic Viral Immunotherapy
by Rakin Tammam Nasar, Ifeanyi Kingsley Uche and Konstantin G. Kousoulas
Curr. Issues Mol. Biol. 2024, 46(6), 5582-5594; https://doi.org/10.3390/cimb46060334 - 3 Jun 2024
Viewed by 606
Abstract
The recent success of cancer immunotherapies, such as immune checkpoint inhibitor (ICIs), monoclonal antibodies (mAbs), cancer vaccines, and adoptive cellular therapies (ACTs), has revolutionized traditional cancer treatment. However, these immunotherapeutic modalities have variable efficacies, and many of them exhibit adverse effects. Oncolytic viral [...] Read more.
The recent success of cancer immunotherapies, such as immune checkpoint inhibitor (ICIs), monoclonal antibodies (mAbs), cancer vaccines, and adoptive cellular therapies (ACTs), has revolutionized traditional cancer treatment. However, these immunotherapeutic modalities have variable efficacies, and many of them exhibit adverse effects. Oncolytic viral Immunotherapy (OViT), whereby viruses are used to directly or indirectly induce anti-cancer immune responses, is emerging as a novel immunotherapy for treating patients with different types of cancer. The herpes simplex virus type-1 (HSV-1) possesses many characteristics that inform its use as an effective OViT agents and remains a leading candidate. Its recent clinical success resulted in the Food and Drug Administration (FDA) approval of Talimogene laherparevec (T-VEC or Imlygic) in 2015 for the treatment of advanced melanoma. In this review, we discuss recent advances in the development of oncolytic HSV-1-based OViTs, their anti-tumor mechanism of action, and efficacy data from recent clinical trials. We envision this knowledge may be used to inform the rational design and application of future oHSV in cancer treatment. Full article
(This article belongs to the Special Issue Research on Virus-Induced Cellular and Molecular Responses)
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17 pages, 1821 KiB  
Review
HIV-1 Structural Proteins or Cell-Signaling Factors? That Is the Question!
by Michele Pellegrino, Francesca Giordano, Francesca De Amicis, Maria Marra, Paola Tucci, Stefania Marsico and Stefano Aquaro
Curr. Issues Mol. Biol. 2024, 46(6), 5100-5116; https://doi.org/10.3390/cimb46060306 - 22 May 2024
Viewed by 802
Abstract
The biological activity of structural HIV-1 proteins is not limited to ensuring a productive viral infection but also interferes with cellular homeostasis through intra- and extracellular signaling activation. This interference induces genomic instability, increases the lifespan of the infected cell by inhibiting apoptosis, [...] Read more.
The biological activity of structural HIV-1 proteins is not limited to ensuring a productive viral infection but also interferes with cellular homeostasis through intra- and extracellular signaling activation. This interference induces genomic instability, increases the lifespan of the infected cell by inhibiting apoptosis, and subverts cell senescence, resulting in unrestricted cell proliferation. HIV structural proteins are present in a soluble form in the lymphoid tissues and blood of infected individuals, even without active viral replication. The HIV matrix protein p17, the envelope glycoprotein gp120, the transenvelope protein gp41, and the capsid protein p24 interact with immune cells and deregulate the biological activity of the immune system. The biological activity of HIV structural proteins is also demonstrated in endothelial cells and some tumor cell lines, confirming the ability of viral proteins to promote cell proliferation and cancer progression, even in the absence of active viral replication. This review corroborates the hypothesis that HIV structural proteins, by interacting with different cell types, contribute to creating a microenvironment that is favorable to the evolution of cancerous pathologies not classically related to AIDS. Full article
(This article belongs to the Special Issue Research on Virus-Induced Cellular and Molecular Responses)
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23 pages, 7534 KiB  
Review
Insights into the Activation of Unfolded Protein Response Mechanism during Coronavirus Infection
by Panagiotis Keramidas, Maria Pitou, Eleni Papachristou and Theodora Choli-Papadopoulou
Curr. Issues Mol. Biol. 2024, 46(5), 4286-4308; https://doi.org/10.3390/cimb46050261 - 5 May 2024
Viewed by 971
Abstract
Coronaviruses represent a significant class of viruses that affect both animals and humans. Their replication cycle is strongly associated with the endoplasmic reticulum (ER), which, upon virus invasion, triggers ER stress responses. The activation of the unfolded protein response (UPR) within infected cells [...] Read more.
Coronaviruses represent a significant class of viruses that affect both animals and humans. Their replication cycle is strongly associated with the endoplasmic reticulum (ER), which, upon virus invasion, triggers ER stress responses. The activation of the unfolded protein response (UPR) within infected cells is performed from three transmembrane receptors, IRE1, PERK, and ATF6, and results in a reduction in protein production, a boost in the ER’s ability to fold proteins properly, and the initiation of ER-associated degradation (ERAD) to remove misfolded or unfolded proteins. However, in cases of prolonged and severe ER stress, the UPR can also instigate apoptotic cell death and inflammation. Herein, we discuss the ER-triggered host responses after coronavirus infection, as well as the pharmaceutical targeting of the UPR as a potential antiviral strategy. Full article
(This article belongs to the Special Issue Research on Virus-Induced Cellular and Molecular Responses)
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