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RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies
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RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies

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

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 18560

Special Issue Editor

Dr. Qibin Geng

E-Mail Website
Guest Editor
Department of Pharmacology, University of Minnesota, Minneapolis, MN 55455, USA
Interests: virus; host; structure; biology; cells; biochemistry; protein; gene; vaccines; immunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, the scientific community has been engrossed in the study of RNA viruses, a critical area of research that has gained unprecedented attention due to the global health crises instigated by these pathogens. RNA viruses, characterized by their complex life cycles and interactions with host cells, have become the epicenter of innovative research that seeks to connect molecular insights with the formulation of effective therapeutic strategies.

This Special Issue seeks to highlight research exploring the molecular mechanisms of RNA viruses, encompassing their complex replication strategies, structural dynamics, and life cycles, as well as their nuanced interaction and modulation of host cellular processes at both cellular and molecular levels. Furthermore, we encourage contributions that venture into potential therapeutic avenues grounded in these molecular insights, encompassing the development of antiviral drugs, vaccines, and novel approaches targeting RNA virus–host interactions.

As we venture further into this field, we aspire to foster a rich dialogue that seamlessly integrates molecular research with the evolution of therapeutic strategies, crafting a comprehensive approach to combating RNA viral infections. This Special Issue serves as a platform for researchers to contribute their original research articles, reviews, and perspectives, with a particular focus on those that resonate with the current trends and prospective directions in the field of RNA virus research.

We eagerly anticipate your invaluable contributions, which promise to shape a robust narrative, fostering innovation and collaboration in the relentless pursuit of mitigating the threats posed by RNA viruses.

Dr. Qibin Geng
Guest Editor

Manuscript Submission Information

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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.

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Keywords

  • RNA virus mechanisms
  • viral pathogenesis
  • host–virus interactions
  • antiviral drug discovery
  • vaccine development
  • RNA virus epidemiology
  • RNA virus structure
  • RNA virus evolution

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Published Papers (6 papers)

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Research

19 pages, 6124 KiB  
Article
HIV Protein Nef Induces Cardiomyopathy Through Induction of Bcl2 and p21
by Olena Kondrachuck, Pierce Ciccone, Nicole Ford, Kim Hong, Yuka Kimura, Jorgo Zi, Sumaya Yusuf, Aya Alkousa, Nishit Tailor, Rithvik Rajkumar, Jay Rappaport and Manish K. Gupta
Int. J. Mol. Sci. 2024, 25(21), 11401; https://doi.org/10.3390/ijms252111401 - 23 Oct 2024
Viewed by 625
Abstract
HIV-associated cardiovascular diseases remain a leading cause of death in people living with HIV/AIDS (PLWHA). Although antiretroviral drugs suppress the viral load, they fail to remove the virus entirely. HIV-1 Nef protein is known to play a role in viral virulence and HIV [...] Read more.
HIV-associated cardiovascular diseases remain a leading cause of death in people living with HIV/AIDS (PLWHA). Although antiretroviral drugs suppress the viral load, they fail to remove the virus entirely. HIV-1 Nef protein is known to play a role in viral virulence and HIV latency. Expression of Nef protein can be detected in different organs, including cardiac tissue. Despite the established role of Nef protein in HIV-1 replication, its impact on organ function inside the human body is not clear. To understand the effect of Nef at the organ level, we created a new Nef-transgenic (Nef-TG) mouse that expresses Nef protein in the heart. Our study found that Nef expression caused inhibition of cardiac function and pathological changes in the heart with increased fibrosis, leading to heart failure and early mortality. Further, we found that cellular autophagy is significantly inhibited in the cardiac tissue of Nef-TG mice. Mechanistically, we found that Nef protein causes the accumulation of Bcl2 and Beclin-1 proteins in the tissue, which may affect the cellular autophagy system. Additionally, we found Nef expression causes upregulation of the cellular senescence marker p21 and senescence-associated β-galactosidase expression. Our findings suggest that the Nef-mediated inhibition of autophagy and induction of senescence markers may promote aging in PLWHA. Our mouse model could help us to understand the effect of Nef protein on organ function during latent HIV infection. Full article
(This article belongs to the Special Issue RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies)
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17 pages, 2834 KiB  
Article
Phase Separation of SARS-CoV-2 Nucleocapsid Protein with TDP-43 Is Dependent on C-Terminus Domains
by Michael J. Strong, Crystal McLellan, Brianna Kaplanis, Cristian A. Droppelmann and Murray Junop
Int. J. Mol. Sci. 2024, 25(16), 8779; https://doi.org/10.3390/ijms25168779 - 12 Aug 2024
Viewed by 1060
Abstract
The SARS-CoV-2 nucleocapsid protein (N protein) is critical in viral replication by undergoing liquid–liquid phase separation to seed the formation of a ribonucleoprotein (RNP) complex to drive viral genomic RNA (gRNA) translation and in suppressing both stress granules and processing bodies, which is [...] Read more.
The SARS-CoV-2 nucleocapsid protein (N protein) is critical in viral replication by undergoing liquid–liquid phase separation to seed the formation of a ribonucleoprotein (RNP) complex to drive viral genomic RNA (gRNA) translation and in suppressing both stress granules and processing bodies, which is postulated to increase uncoated gRNA availability. The N protein can also form biomolecular condensates with a broad range of host endogenous proteins including RNA binding proteins (RBPs). Amongst these RBPs are proteins that are associated with pathological, neuronal, and glial cytoplasmic inclusions across several adult-onset neurodegenerative disorders, including TAR DNA binding protein 43 kDa (TDP-43) which forms pathological inclusions in over 95% of amyotrophic lateral sclerosis cases. In this study, we demonstrate that the N protein can form biomolecular condensates with TDP-43 and that this is dependent on the N protein C-terminus domain (N-CTD) and the intrinsically disordered C-terminus domain of TDP-43. This process is markedly accelerated in the presence of RNA. In silico modeling suggests that the biomolecular condensate that forms in the presence of RNA is composed of an N protein quadriplex in which the intrinsically disordered TDP-43 C terminus domain is incorporated. Full article
(This article belongs to the Special Issue RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies)
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20 pages, 6103 KiB  
Communication
Redox Homeostasis Alteration Is Restored through Melatonin Treatment in COVID-19 Patients: A Preliminary Study
by María Elena Soto, Israel Pérez-Torres, Linaloe Manzano-Pech, Adrían Palacios-Chavarría, Rafael Ricardo Valdez-Vázquez, Verónica Guarner-Lans, Elizabeth Soria-Castro, Eulises Díaz-Díaz and Vicente Castrejón-Tellez
Int. J. Mol. Sci. 2024, 25(8), 4543; https://doi.org/10.3390/ijms25084543 - 21 Apr 2024
Cited by 2 | Viewed by 1521
Abstract
Type II pneumocytes are the target of the SARS-CoV-2 virus, which alters their redox homeostasis to increase reactive oxygen species (ROS). Melatonin (MT) has antioxidant proprieties and protects mitochondrial function. In this study, we evaluated whether treatment with MT compensated for the redox [...] Read more.
Type II pneumocytes are the target of the SARS-CoV-2 virus, which alters their redox homeostasis to increase reactive oxygen species (ROS). Melatonin (MT) has antioxidant proprieties and protects mitochondrial function. In this study, we evaluated whether treatment with MT compensated for the redox homeostasis alteration in serum from COVID-19 patients. We determined oxidative stress (OS) markers such as carbonyls, glutathione (GSH), total antioxidant capacity (TAC), thiols, nitrites (NO2−), lipid peroxidation (LPO), and thiol groups in serum. We also studied the enzymatic activities of glutathione peroxidase (GPx), glutathione-S-transferase (GST), reductase (GR), thioredoxin reductase (TrxR), extracellular superoxide dismutase (ecSOD) and peroxidases. There were significant increases in LPO and carbonyl quantities (p ≤ 0.03) and decreases in TAC and the quantities of NO2−, thiols, and GSH (p < 0.001) in COVID-19 patients. The activities of the antioxidant enzymes such as ecSOD, TrxR, GPx, GST, GR, and peroxidases were decreased (p ≤ 0.04) after the MT treatment. The treatment with MT favored the activity of the antioxidant enzymes that contributed to an increase in TAC and restored the lost redox homeostasis. MT also modulated glucose homeostasis, functioning as a glycolytic agent, and inhibited the Warburg effect. Thus, MT restores the redox homeostasis that is altered in COVID-19 patients and can be used as adjuvant therapy in SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies)
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29 pages, 3881 KiB  
Article
1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit
by Jozef Nahalka
Int. J. Mol. Sci. 2024, 25(8), 4440; https://doi.org/10.3390/ijms25084440 - 18 Apr 2024
Cited by 1 | Viewed by 1554
Abstract
The COVID-19 pandemic prompted rapid research on SARS-CoV-2 pathogenicity. Consequently, new data can be used to advance the molecular understanding of SARS-CoV-2 infection. The present bioinformatics study discusses the “spikeopathy” at the molecular level and focuses on the possible post-transcriptional regulation of the [...] Read more.
The COVID-19 pandemic prompted rapid research on SARS-CoV-2 pathogenicity. Consequently, new data can be used to advance the molecular understanding of SARS-CoV-2 infection. The present bioinformatics study discusses the “spikeopathy” at the molecular level and focuses on the possible post-transcriptional regulation of the SARS-CoV-2 spike protein S1 subunit in the host cell/tissue. A theoretical protein–RNA recognition code was used to check the compatibility of the SARS-CoV-2 spike protein S1 subunit with mRNAs in the human transcriptome (1-L transcription). The principle for this method is elucidated on the defined RNA binding protein GEMIN5 (gem nuclear organelle-associated protein 5) and RNU2-1 (U2 spliceosomal RNA). Using the method described here, it was shown that 45% of the genes/proteins identified by 1-L transcription of the SARS-CoV-2 spike protein S1 subunit are directly linked to COVID-19, 39% are indirectly linked to COVID-19, and 16% cannot currently be associated with COVID-19. The identified genes/proteins are associated with stroke, diabetes, and cardiac injury. Full article
(This article belongs to the Special Issue RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies)
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34 pages, 5189 KiB  
Article
Bioinformatics Insights on Viral Gene Expression Transactivation: From HIV-1 to SARS-CoV-2
by Roberto Patarca and William A. Haseltine
Int. J. Mol. Sci. 2024, 25(6), 3378; https://doi.org/10.3390/ijms25063378 - 16 Mar 2024
Cited by 1 | Viewed by 1822
Abstract
Viruses provide vital insights into gene expression control. Viral transactivators, with other viral and cellular proteins, regulate expression of self, other viruses, and host genes with profound effects on infected cells, underlying inflammation, control of immune responses, and pathogenesis. The multifunctional Tat proteins [...] Read more.
Viruses provide vital insights into gene expression control. Viral transactivators, with other viral and cellular proteins, regulate expression of self, other viruses, and host genes with profound effects on infected cells, underlying inflammation, control of immune responses, and pathogenesis. The multifunctional Tat proteins of lentiviruses (HIV-1, HIV-2, and SIV) transactivate gene expression by recruiting host proteins and binding to transacting responsive regions (TARs) in viral and host RNAs. SARS-CoV-2 nucleocapsid participates in early viral transcription, recruits similar cellular proteins, and shares intracellular, surface, and extracellular distribution with Tat. SARS-CoV-2 nucleocapsid interacting with the replication–transcription complex might, therefore, transactivate viral and cellular RNAs in the transcription and reactivation of self and other viruses, acute and chronic pathogenesis, immune evasion, and viral evolution. Here, we show, by using primary and secondary structural comparisons, that the leaders of SARS-CoV-2 and other coronaviruses contain TAR-like sequences in stem-loops 2 and 3. The coronaviral nucleocapsid C-terminal domains harbor a region of similarity to TAR-binding regions of lentiviral Tat proteins, and coronaviral nonstructural protein 12 has a cysteine-rich metal binding, dimerization domain, as do lentiviral Tat proteins. Although SARS-CoV-1 nucleocapsid transactivated gene expression in a replicon-based study, further experimental evidence for coronaviral transactivation and its possible implications is warranted. Full article
(This article belongs to the Special Issue RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies)
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14 pages, 1555 KiB  
Article
In-Host HEV Quasispecies Evolution Shows the Limits of Mutagenic Antiviral Treatments
by Sergi Colomer-Castell, Josep Gregori, Damir Garcia-Cehic, Mar Riveiro-Barciela, Maria Buti, Ariadna Rando-Segura, Judit Vico-Romero, Carolina Campos, Marta Ibañez-Lligoña, Caroline Melanie Adombi, Maria Francesca Cortese, David Tabernero, Juan Ignacio Esteban, Francisco Rodriguez-Frias and Josep Quer
Int. J. Mol. Sci. 2023, 24(24), 17185; https://doi.org/10.3390/ijms242417185 - 6 Dec 2023
Cited by 3 | Viewed by 1224
Abstract
Here, we report the in-host hepatitis E virus (HEV) quasispecies evolution in a chronically infected patient who was treated with three different regimens of ribavirin (RBV) for nearly 6 years. Sequential plasma samples were collected at different time points and subjected to RNA [...] Read more.
Here, we report the in-host hepatitis E virus (HEV) quasispecies evolution in a chronically infected patient who was treated with three different regimens of ribavirin (RBV) for nearly 6 years. Sequential plasma samples were collected at different time points and subjected to RNA extraction and deep sequencing using the MiSeq Illumina platforms. Specifically, we RT-PCR amplified a single amplicon from the core region located in the open-reading frame 2 (ORF2). At the nucleotide level (genotype), our analysis showed an increase in the number of rare haplotypes and a drastic reduction in the frequency of the master (most represented) sequence during the period when the virus was found to be insensitive to RBV treatment. Contrarily, at the amino acid level (phenotype), our study revealed conservation of the amino acids, which is represented by a high prevalence of the master sequence. Our findings suggest that using mutagenic antivirals concomitant with high viral loads can lead to the selection and proliferation of a rich set of synonymous haplotypes that express the same phenotype. This can also lead to the selection and proliferation of conservative substitutions that express fitness-enhanced phenotypes. These results have important clinical implications, as they suggest that using mutagenic agents as a monotherapy treatment regimen in the absence of sufficiently effective viral inhibitors can result in diversification and proliferation of a highly diverse quasispecies resistant to further treatment. Therefore, such approaches should be avoided whenever possible. Full article
(This article belongs to the Special Issue RNA Virus Mechanisms: From Molecular Insights to Therapeutic Strategies)
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