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Viruses
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Host Cell-Virus Interaction, 3rd Edition
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Host Cell-Virus Interaction, 3rd Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 20120

Special Issue Editors

Dr. Parikshit Bagchi

E-Mail Website
Guest Editor
Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA
Interests: host cell-virus interaction; intracellular trafficking of virus; membrane trafficking; non-enveloped viruses; positive sense RNA viruses
Special Issues, Collections and Topics in MDPI journals
Dr. Anupam Mukherjee

E-Mail Website
Guest Editor
Division of Virology, ICMR-National AIDS Research Institute, Pune 411026, Maharashtra, India
Interests: RNA virus; viral pathogenesis; host cell–virus interaction; RNAi; small RNA as therapeutics; targeted delivery; virus and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Activation of immune responses is the key factor for host defense against any viral infections. Yet, viruses have also adapted several strategies to escape or suppress host resistance to make a proviral environment using the cellular machineries that represent the most important components of viral pathogenicity. As an obligate parasite, viruses are eventually reliant on the host cellular components for their replication via altering the cellular signal transduction pathways and immune evasion mechanisms, including escaping recognition from intracellular sensors, suppression of IFN-α/β production, NF-kappaB, dysregulation of inflammatory responses and inflammasome activation signals, RNA interference, modulation of autophagy and programmed cell-death mechanisms, and selection of genetic variants that escape from neutralizing antibodies.

Significant research on antivirals to combat viral infections is an extensive process, which requires multidisciplinary approaches. For any antiviral agents, such as synthetic drugs, chemical inhibitors, RNAi strategies of miRNAs or siRNAs, natural compounds, phytoconstituents, herbal or Ayurvedic formulations, and metallic nanoparticles, apparently there are two different strategies of antiviral drug discovery available, which are based on targeting the viral lifecycle and/or directing the host cellular factors. The modus operandi of antivirals characterization is fundamental for identification, prediction and understanding side-effects, drug interactions and the emergence of resistance, for increasing the spectrum of activity, and for improving antiviral efficacy.

For this Special Issue, we welcome original research papers, communications and review articles that contribute to an improved understanding of the molecular details of host cell–virus interaction through viral immune evasion and host defense mechanism during any viral infection. Furthermore, understanding the mechanism of action of host-centric and/or targeting viral lifecycle antivirals could further refine our understanding of virus–host interactions and the antiviral strategies for treatment and prophylaxis, which are essential to managing any active viral infections. Hence, we invite all researchers working in the field of viral lifecycle, pathogenesis, host responses and antiviral development to submit their research to this Special Issue to highlight recent advancements and further the discussion on host–virus interactions and prospective therapeutics.

Dr. Parikshit Bagchi
Dr. Anupam Mukherjee
Guest Editors

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. 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

  • virus
  • viral proteins
  • virus entry
  • viral replication and pathogenesis
  • virus assembly and egress
  • intracellular trafficking of virus
  • host cell
  • cellular signaling
  • interferon pathway
  • inflammasome
  • viral immune evasion
  • immune response
  • cell death
  • apoptosis
  • autophagy
  • host-virus interaction
  • anti-viral strategies
  • direct acting antivirals
  • broad-spectrum antiviral agents
  • RNAi
  • microRNAs
  • neutralizing antibodies
  • molecular mechanisms of antivirals
  • molecular mechanisms of drug-resistance

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Published Papers (14 papers)

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Editorial

Jump to: Research, Review, Other

3 pages, 159 KiB  
Editorial
Exploring the Frontiers of Virus–Host Interactions—3rd Edition
by Anupam Mukherjee and Parikshit Bagchi
Viruses 2024, 16(10), 1544; https://doi.org/10.3390/v16101544 - 30 Sep 2024
Viewed by 571
Abstract
It is with great enthusiasm that we introduce the third edition of the “Virus–Host Interaction” series, a collection that epitomizes the ever-evolving landscape of virology [...] Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)

Research

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14 pages, 3745 KiB  
Article
Sputnik V-Induced Antibodies against SARS-CoV-2 Variants during the Dissemination of the Gamma Variant in Venezuela
by Christopher Franco, Alejandro Cornejo, Mariajosé Rodríguez, Alexis García, Inirida Belisario, Soriuska Mayora, Domingo José Garzaro, Rossana Celeste Jaspe, Mariana Hidalgo, Nereida Parra, Ferdinando Liprandi, José Luis Zambrano, Héctor Rafael Rangel and Flor Helene Pujol
Viruses 2024, 16(9), 1480; https://doi.org/10.3390/v16091480 - 18 Sep 2024
Cited by 1 | Viewed by 895
Abstract
The COVID-19 pandemic was characterized by the emergence and succession of SARS-CoV-2 variants able to evade the antibody response induced by natural infection and vaccination. To evaluate the IgG reactivity and neutralizing capacity of the serum of individuals vaccinated with Sputnik V (105 [...] Read more.
The COVID-19 pandemic was characterized by the emergence and succession of SARS-CoV-2 variants able to evade the antibody response induced by natural infection and vaccination. To evaluate the IgG reactivity and neutralizing capacity of the serum of individuals vaccinated with Sputnik V (105 volunteers vaccinated) against different viral variants. IgG reactivity to the Spike protein (S) was evaluated by ELISA. A plaque reduction neutralization test was performed using different viral variant isolates. At 42 days post-vaccination, the frequency of recognition and reactivity to the S protein of the Omicron variant was lower compared to that of the other variants. In general, a higher average neutralization titer was seen against the ancestral variant compared to the variants, especially Omicron. However, some sera exhibited a higher neutralization titer to the Gamma variant compared to the ancestral variant, suggesting unapparent exposure during the clinical trial. Antibodies induced by Sputnik V can recognize, persist, and neutralize SARS-CoV-2 variants, with Omicron being the one that best evades this response. These results represent a unique report on the humoral response induced by a globally lesser-studied vaccine in terms of efficacy and immune escape, offering insights into developing vaccines targeting unknown coronaviruses. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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22 pages, 3652 KiB  
Article
Metabolic Dependency Shapes Bivalent Antiviral Response in Host Cells in Response to Poly:IC: The Role of Glutamine
by Grégorie Lebeau, Aurélie Paulo-Ramos, Mathilde Hoareau, Daed El Safadi, Olivier Meilhac, Pascale Krejbich-Trotot, Marjolaine Roche and Wildriss Viranaicken
Viruses 2024, 16(9), 1391; https://doi.org/10.3390/v16091391 - 30 Aug 2024
Cited by 3 | Viewed by 720
Abstract
The establishment of effective antiviral responses within host cells is intricately related to their metabolic status, shedding light on immunometabolism. In this study, we investigated the hypothesis that cellular reliance on glutamine metabolism contributes to the development of a potent antiviral response. We [...] Read more.
The establishment of effective antiviral responses within host cells is intricately related to their metabolic status, shedding light on immunometabolism. In this study, we investigated the hypothesis that cellular reliance on glutamine metabolism contributes to the development of a potent antiviral response. We evaluated the antiviral response in the presence or absence of L-glutamine in the culture medium, revealing a bivalent response hinging on cellular metabolism. While certain interferon-stimulated genes (ISGs) exhibited higher expression in an oxidative phosphorylation (OXPHOS)-dependent manner, others were surprisingly upregulated in a glycolytic-dependent manner. This metabolic dichotomy was influenced in part by variations in interferon-β (IFN-β) expression. We initially demonstrated that the presence of L-glutamine induced an enhancement of OXPHOS in A549 cells. Furthermore, in cells either stimulated by poly:IC or infected with dengue virus and Zika virus, a marked increase in ISGs expression was observed in a dose-dependent manner with L-glutamine supplementation. Interestingly, our findings unveiled a metabolic dependency in the expression of specific ISGs. In particular, genes such as ISG54, ISG12 and ISG15 exhibited heightened expression in cells cultured with L-glutamine, corresponding to higher OXPHOS rates and IFN-β signaling. Conversely, the expression of viperin and 2′-5′-oligoadenylate synthetase 1 was inversely related to L-glutamine concentration, suggesting a glycolysis-dependent regulation, confirmed by inhibition experiments. This study highlights the intricate interplay between cellular metabolism, especially glutaminergic and glycolytic, and the establishment of the canonical antiviral response characterized by the expression of antiviral effectors, potentially paving the way for novel strategies to modulate antiviral responses through metabolic interventions. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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20 pages, 2558 KiB  
Article
HSV-2 Manipulates Autophagy through Interferon Pathway: A Strategy for Viral Survival
by Debashree Dass, Anwesha Banerjee, Kishore Dhotre, Vaishnavi Sonawane, Ashwini More and Anupam Mukherjee
Viruses 2024, 16(9), 1383; https://doi.org/10.3390/v16091383 - 29 Aug 2024
Cited by 1 | Viewed by 788
Abstract
Autophagy, an evolutionarily conserved cellular process, influences the regulation of viral infections. While the existing understanding indicates that Herpes Simplex Virus type 2 (HSV-2) maintains a basal level of autophagy to support its viral yield, the precise pathways governing the induction of autophagy [...] Read more.
Autophagy, an evolutionarily conserved cellular process, influences the regulation of viral infections. While the existing understanding indicates that Herpes Simplex Virus type 2 (HSV-2) maintains a basal level of autophagy to support its viral yield, the precise pathways governing the induction of autophagy during HSV-2 infection remain unknown. Therefore, this study aims to explore the role of type I interferons (IFN-I) in modulating autophagy during HSV-2 infection and to decode the associated signaling pathways. Our findings revealed an interplay wherein IFN-I regulates the autophagic response during HSV-2 infection. Additionally, we investigated the cellular pathways modulated during this complex process. Exploring the intricate network of signaling events involved in autophagy induction during HSV-2 infection holds promising therapeutic implications. Identifying these pathways advances our understanding of host–virus interactions and holds the foundation for developing targeted therapeutic strategies against HSV-2. The insight gained from this study provides a platform for exploring potential therapeutic targets to restrict HSV-2 infections, addressing a crucial need in antiviral research. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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13 pages, 3997 KiB  
Article
Effect of Heat Shock Treatment on the Virulence of Grass Carp Reovirus in Rare Minnow Gobiocypris rarus
by Qinwei Ni, Yanchang Fan, Simin Xiao and Liqun Lu
Viruses 2024, 16(6), 921; https://doi.org/10.3390/v16060921 - 5 Jun 2024
Cited by 1 | Viewed by 820
Abstract
The mode and outcome of fish–virus interactions are influenced by many abiotic factors, among which water temperature is especially important in poikilothermic fish. Rare minnow Gobiocypris rarus is a eurythermal small cyprinid fish that is sensitive to infection with genotype II grass carp [...] Read more.
The mode and outcome of fish–virus interactions are influenced by many abiotic factors, among which water temperature is especially important in poikilothermic fish. Rare minnow Gobiocypris rarus is a eurythermal small cyprinid fish that is sensitive to infection with genotype II grass carp reovirus (GCRV). HSP70, a conservative and key player in heat shock response, is previously identified as an induced pro-viral factor during GCRV infection in vitro. Here, rare minnow was subjected to heat shock treatment (HST), 1 h treatment at 32 °C followed by reverting to a normal temperature of 24 °C, and subsequently challenged with GCRV-II at a dosage of 1 × LD50. The effect of HST on GCRV virulence in vivo was evaluated by calculating virus-associated mortality and viral load in both dead and survival fish. The results revealed that HST enhanced the mortality of rare minnow infected with GCRV; the fact that viral loads in the tissue samples of HST-treated fish were significantly higher than those in samples of the control group at 6, 8 d p.i. reflected a faster infection process due to HST. Quantitative gene expression analysis was further employed to show that the expression levels of Hsp70 in intestine and liver tissues from the HST group declined faster than muscle tissue after HST. HST W/O GCRV challenge upregulated proinflammatory cytokines such as MyD88 and Nf-κB, which was in consistence with the inflammation observed in histopathological analysis. This study shed light on the complexity of the interaction between fish abiotic and biotic stress response, which suggested that HST, an abiotic stress, could enhance the virulence of GCRV in Gobiocypris rarus that involved modulating the gene expression of host heat shock, as well as a pro-inflammatory response. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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50 pages, 9208 KiB  
Article
Intrinsic Disorder in the Host Proteins Entrapped in Rabies Virus Particles
by Hafiza Nimra Ashraf and Vladimir N. Uversky
Viruses 2024, 16(6), 916; https://doi.org/10.3390/v16060916 - 4 Jun 2024
Cited by 1 | Viewed by 1923
Abstract
A proteomics analysis of purified rabies virus (RABV) revealed 47 entrapped host proteins within the viral particles. Out of these, 11 proteins were highly disordered. Our study was particularly focused on five of the RABV-entrapped mouse proteins with the highest levels of disorder: [...] Read more.
A proteomics analysis of purified rabies virus (RABV) revealed 47 entrapped host proteins within the viral particles. Out of these, 11 proteins were highly disordered. Our study was particularly focused on five of the RABV-entrapped mouse proteins with the highest levels of disorder: Neuromodulin, Chmp4b, DnaJB6, Vps37B, and Wasl. We extensively utilized bioinformatics tools, such as FuzDrop, D2P2, UniProt, RIDAO, STRING, AlphaFold, and ELM, for a comprehensive analysis of the intrinsic disorder propensity of these proteins. Our analysis suggested that these disordered host proteins might play a significant role in facilitating the rabies virus pathogenicity, immune system evasion, and the development of antiviral drug resistance. Our study highlighted the complex interaction of the virus with its host, with a focus on how the intrinsic disorder can play a crucial role in virus pathogenic processes, and suggested that these intrinsically disordered proteins (IDPs) and disorder-related host interactions can also be a potential target for therapeutic strategies. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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16 pages, 4289 KiB  
Article
Mathematical Modeling Suggests That Monocyte Activity May Drive Sex Disparities during Influenza Infection
by Tatum S. Liparulo and Jason E. Shoemaker
Viruses 2024, 16(6), 837; https://doi.org/10.3390/v16060837 - 24 May 2024
Cited by 1 | Viewed by 1053
Abstract
In humans, females of reproductive age often experience a more severe disease during influenza A virus infection, which may be due to differences in their innate immune response. Sex-specific outcomes to influenza infection have been recapitulated in mice, enabling researchers to study viral [...] Read more.
In humans, females of reproductive age often experience a more severe disease during influenza A virus infection, which may be due to differences in their innate immune response. Sex-specific outcomes to influenza infection have been recapitulated in mice, enabling researchers to study viral and immune dynamics in vivo in order to identify immune mechanisms that are differently regulated between the sexes. This study is based on the hypothesis that sex-specific outcomes emerge due to differences in the rates/speeds that select immune components respond. Using publicly available sex-specific murine data, we utilized dynamic mathematical models of the innate immune response to identify candidate mechanisms that may lead to increased disease severity in female mice. We implemented a large computational screen using the Bayesian information criterion (BIC), wherein the goodness of fit of the competing model scenarios is balanced against complexity (i.e., the number of parameters). Our results suggest that having sex-specific rates for proinflammatory monocyte induction by interferon and monocyte inhibition of virus replication provides the simplest (lowest BIC) explanation for the difference observed in the male and female immune responses. Markov-chain Monte Carlo (MCMC) analysis and global sensitivity analysis of the top performing scenario were performed to provide rigorous estimates of the sex-specific parameter distributions and to provide insight into which parameters most affect innate immune responses. Simulations using the top-performing model suggest that monocyte activity could be a key target to reduce influenza disease severity in females. Overall, our Bayesian statistical and dynamic modeling approach suggests that monocyte activity and induction parameters are sex-specific and may explain sex-differences in influenza disease immune dynamics. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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13 pages, 1868 KiB  
Article
CRISPR Screen Reveals PACT as a Pro-Viral Factor for Dengue Viral Replication
by Shwetha Shivaprasad, Wenjie Qiao, Kuo-Feng Weng, Pavithra Umashankar, Jan E. Carette and Peter Sarnow
Viruses 2024, 16(5), 725; https://doi.org/10.3390/v16050725 - 3 May 2024
Cited by 2 | Viewed by 1977
Abstract
The dengue virus is a single-stranded, positive-sense RNA virus that infects ~400 million people worldwide. Currently, there are no approved antivirals available. CRISPR-based screening methods have greatly accelerated the discovery of host factors that are essential for DENV infection and that can be [...] Read more.
The dengue virus is a single-stranded, positive-sense RNA virus that infects ~400 million people worldwide. Currently, there are no approved antivirals available. CRISPR-based screening methods have greatly accelerated the discovery of host factors that are essential for DENV infection and that can be targeted in host-directed antiviral interventions. In the present study, we performed a focused CRISPR (Clustered Regularly Interspaced Palindromic Repeats) library screen to discover the key host factors that are essential for DENV infection in human Huh7 cells and identified the Protein Activator of Interferon-Induced Protein Kinase (PACT) as a novel pro-viral factor for DENV. PACT is a double-stranded RNA-binding protein generally known to activate antiviral responses in virus-infected cells and block viral replication. However, in our studies, we observed that PACT plays a pro-viral role in DENV infection and specifically promotes viral RNA replication. Knockout of PACT resulted in a significant decrease in DENV RNA and protein abundances in infected cells, which was rescued upon ectopic expression of full-length PACT. An analysis of global gene expression changes indicated that several ER-associated pro-viral genes such as ERN1, DDIT3, HERPUD1, and EIF2AK3 are not upregulated in DENV-infected PACT knockout cells as compared to infected wildtype cells. Thus, our study demonstrates a novel role for PACT in promoting DENV replication, possibly through modulating the expression of ER-associated pro-viral genes. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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16 pages, 7272 KiB  
Article
Genetic and Biological Characteristics of Duck-Origin H4N6 Avian Influenza Virus Isolated in China in 2022
by Tian Li, Chuankuo Zhao, Yuxin Guo, Jinze Dong, Fanshu Du, Yong Zhou, Sicheng Shu, Yang Liu, Yachang Cheng, Zhiyong Cao, Qi Cao, Shuiping Shi, Yinhua Huang, Juan Pu and Litao Liu
Viruses 2024, 16(2), 207; https://doi.org/10.3390/v16020207 - 30 Jan 2024
Cited by 1 | Viewed by 1882
Abstract
The interaction between migratory birds and domestic waterfowl facilitates viral co-infections, leading to viral reassortment and the emergence of novel viruses. In 2022, samples were collected from duck farms around Poyang Lake in Jiangxi Province, China, which is located within the East Asia–Australasia [...] Read more.
The interaction between migratory birds and domestic waterfowl facilitates viral co-infections, leading to viral reassortment and the emergence of novel viruses. In 2022, samples were collected from duck farms around Poyang Lake in Jiangxi Province, China, which is located within the East Asia–Australasia flyway. Three strains of H4N6 avian influenza virus (AIV) were isolated. Genetic and phylogenetic analyses showed that the isolated H4N6 avian influenza viruses (AIVs) belonged to new genotypes, G23 and G24. All isolated strains demonstrated dual receptor binding properties. Additionally, the isolated strains were able to replicate efficiently not only in avian cells but also in mammalian cells. Furthermore, the H4N6 AIV isolates could infect chickens, with viral replication detected in the lungs and extrapulmonary organs, and could transmit within chicken flocks through contact, with viral shedding detected only in oropharyngeal swabs from chickens in the contact group. Notably, the H4N6 AIV could infect mice without prior adaptation and replicate in the lungs with high viral titers, suggesting that it is a potential threat to humans. In conclusion, this study provides valuable insight into the characteristics of H4N6 strains currently circulating in China. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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17 pages, 4207 KiB  
Article
Early Emerging SARS-CoV-2 Spike Mutants Are Diversified in Virologic Properties but Elicit Compromised Antibody Responses
by Junhao Fan, Shixiong Li, Yao Zhang, Jihao Zheng, Dongfang Wang, Yunxi Liao, Zhibo Cui, Dongyu Zhao, Dan H. Barouch and Jingyou Yu
Viruses 2023, 15(12), 2401; https://doi.org/10.3390/v15122401 - 9 Dec 2023
Cited by 2 | Viewed by 1605
Abstract
Despite the effective antivirals and vaccines, COVID-19 remains a public health concern. The mutations that occurred during the early stage of the pandemic can be valuable in assessing the viral fitness and evolutionary trajectory. In this study, we analyzed a panel of 2969 [...] Read more.
Despite the effective antivirals and vaccines, COVID-19 remains a public health concern. The mutations that occurred during the early stage of the pandemic can be valuable in assessing the viral fitness and evolutionary trajectory. In this study, we analyzed a panel of 2969 spike sequences deposited in GISAID before April 2020 and characterized nine representative spike single-point mutants in detail. Compared with the WA01/2020, most (8 out of 9) mutants demonstrated an equivalent or diminished protein expression or processing, pseudovirus infectivity, and cell–cell fusion. Interestingly, most of the mutants in native form elicited minimum antibody responses in mice despite unaltered CD4+ and CD8+ T cell responses. The mutants remained sensitive to the antisera and the type I interferon. Taken together, these data suggest that the early emerging mutants are virologically divergent, and some of which showed transmission fitness. Our findings have important implications for the retrospective tracing of the early SARS-CoV-2 transmission and future pandemic preparedness. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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Review

Jump to: Editorial, Research, Other

20 pages, 1547 KiB  
Review
Unveiling the Connection: Viral Infections and Genes in dNTP Metabolism
by Shih-Yen Lo, Meng-Jiun Lai, Chee-Hing Yang and Hui-Chun Li
Viruses 2024, 16(9), 1412; https://doi.org/10.3390/v16091412 - 3 Sep 2024
Cited by 1 | Viewed by 1325
Abstract
Deoxynucleoside triphosphates (dNTPs) are crucial for the replication and maintenance of genomic information within cells. The balance of the dNTP pool involves several cellular enzymes, including dihydrofolate reductase (DHFR), ribonucleotide reductase (RNR), and SAM and HD domain-containing protein 1 (SAMHD1), among others. DHFR [...] Read more.
Deoxynucleoside triphosphates (dNTPs) are crucial for the replication and maintenance of genomic information within cells. The balance of the dNTP pool involves several cellular enzymes, including dihydrofolate reductase (DHFR), ribonucleotide reductase (RNR), and SAM and HD domain-containing protein 1 (SAMHD1), among others. DHFR is vital for the de novo synthesis of purines and deoxythymidine monophosphate, which are necessary for DNA synthesis. SAMHD1, a ubiquitously expressed deoxynucleotide triphosphohydrolase, converts dNTPs into deoxynucleosides and inorganic triphosphates. This process counteracts the de novo dNTP synthesis primarily carried out by RNR and cellular deoxynucleoside kinases, which are most active during the S phase of the cell cycle. The intracellular levels of dNTPs can influence various viral infections. This review provides a concise summary of the interactions between different viruses and the genes involved in dNTP metabolism. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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25 pages, 1389 KiB  
Review
Toward a Categorization of Virus-ncRNA Interactions in the World of RNA to Disentangle the Tiny Secrets of Dengue Virus
by Clara Isabel Bermudez-Santana and Juan Carlos Gallego-Gómez
Viruses 2024, 16(5), 804; https://doi.org/10.3390/v16050804 - 18 May 2024
Cited by 2 | Viewed by 1381
Abstract
In recent years, the function of noncoding RNAs (ncRNAs) as regulatory molecules of cell physiology has begun to be better understood. Advances in viral molecular biology have shown that host ncRNAs, cellular factors, and virus-derived ncRNAs and their interplay are strongly disturbed during [...] Read more.
In recent years, the function of noncoding RNAs (ncRNAs) as regulatory molecules of cell physiology has begun to be better understood. Advances in viral molecular biology have shown that host ncRNAs, cellular factors, and virus-derived ncRNAs and their interplay are strongly disturbed during viral infections. Nevertheless, the folding of RNA virus genomes has also been identified as a critical factor in regulating canonical and non-canonical functions. Due to the influence of host ncRNAs and the structure of RNA viral genomes, complex molecular and cellular processes in infections are modulated. We propose three main categories to organize the current information about RNA–RNA interactions in some well-known human viruses. The first category shows examples of host ncRNAs associated with the immune response triggered in viral infections. Even though miRNAs introduce a standpoint, they are briefly presented to keep researchers moving forward in uncovering other RNAs. The second category outlines interactions between virus-host ncRNAs, while the third describes how the structure of the RNA viral genome serves as a scaffold for processing virus-derived RNAs. Our grouping may provide a comprehensive framework to classify ncRNA–host-cell interactions for emerging viruses and diseases. In this sense, we introduced them to organize DENV–host-cell interactions. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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21 pages, 2549 KiB  
Review
Potential Pathways and Pathophysiological Implications of Viral Infection-Driven Activation of Kallikrein–Kinin System (KKS)
by Sharton Vinícius Antunes Coelho, Fabiane Messner Augusto and Luciana Barros de Arruda
Viruses 2024, 16(2), 245; https://doi.org/10.3390/v16020245 - 3 Feb 2024
Cited by 2 | Viewed by 1885
Abstract
Microcirculatory and coagulation disturbances commonly occur as pathological manifestations of systemic viral infections. Research exploring the role of the kallikrein–kinin system (KKS) in flavivirus infections has recently linked microvascular dysfunctions to bradykinin (BK)-induced signaling of B2R, a G protein-coupled receptor (GPCR) constitutively expressed [...] Read more.
Microcirculatory and coagulation disturbances commonly occur as pathological manifestations of systemic viral infections. Research exploring the role of the kallikrein–kinin system (KKS) in flavivirus infections has recently linked microvascular dysfunctions to bradykinin (BK)-induced signaling of B2R, a G protein-coupled receptor (GPCR) constitutively expressed by endothelial cells. The relevance of KKS activation as an innate response to viral infections has gained increasing attention, particularly after the reports regarding thrombogenic events during COVID-19. BK receptor (B2R and B1R) signal transduction results in vascular permeability, edema formation, angiogenesis, and pain. Recent findings unveiling the role of KKS in viral pathogenesis include evidence of increased activation of KKS with elevated levels of BK and its metabolites in both intravascular and tissue milieu, as well as reports demonstrating that virus replication stimulates BKR expression. In this review, we will discuss the mechanisms triggered by virus replication and by virus-induced inflammatory responses that may stimulate KKS. We also explore how KKS activation and BK signaling may impact virus pathogenesis and further discuss the potential therapeutic application of BKR antagonists in the treatment of hemorrhagic and respiratory diseases. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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Other

9 pages, 1408 KiB  
Perspective
A Second Career for p53 as A Broad-Spectrum Antiviral?
by Joe B. Harford
Viruses 2023, 15(12), 2377; https://doi.org/10.3390/v15122377 - 3 Dec 2023
Cited by 2 | Viewed by 1780
Abstract
As the world exits the global pandemic caused by the previously unknown SARS-CoV-2, we also mark the 30th anniversary of p53 being named “molecule of the year” by Science based on its role as a tumor suppressor. Although p53 was originally discovered in [...] Read more.
As the world exits the global pandemic caused by the previously unknown SARS-CoV-2, we also mark the 30th anniversary of p53 being named “molecule of the year” by Science based on its role as a tumor suppressor. Although p53 was originally discovered in association with a viral protein, studies on its role in preventing carcinogenesis have far overshadowed research related to p53′s role in viral infections. Nonetheless, there is an extensive body of scientific literature demonstrating that p53 is a critical component of host immune responses to viral infections. It is striking that diverse viruses have independently developed an impressive repertoire of varied mechanisms to counter the host defenses that are mediated by and through p53. The variety of ways developed by viruses to disrupt p53 in their hosts attests to the protein’s importance in combatting viral pathogens. The present perspective aims to make the case that p53 ought to be considered a virus suppressor in addition to a tumor suppressor. It is hoped that additional research aimed at more fully understanding the role of p53 in antiviral immunity will result in the world being better positioned for the next pandemic than it was when SARS-CoV-2 emerged to produce COVID-19. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 3rd Edition)
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