Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.1
4.7
Journals
Viruses
Special Issues
Host Cell–Virus Interaction 2.0
share announcement

Host Cell–Virus Interaction 2.0

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 (30 June 2023) | Viewed by 26988

Special Issue Editors

Dr. Parikshit Bagchi

E-Mail Website
Guest Editor
Department of Molecular Microbiology, Washington University in St. Louis, St. Louis, MO 63130, 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, Maharashtra 411026, 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

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. 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

Published Papers (14 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review, Other

3 pages, 169 KiB  
Editorial
Host Cell–Virus Interaction 2.0: Viral Stratagems of Immune Evasion, Host Cellular Responses and Antiviral Counterattacks
by Anupam Mukherjee and Parikshit Bagchi
Viruses 2023, 15(8), 1717; https://doi.org/10.3390/v15081717 - 10 Aug 2023
Viewed by 713
Abstract
As rightly stated by the author Mira Grant in her novel Countdown, “There is nothing so patient, in this world or any other, as a virus searching for a host” [...] Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)

Research

Jump to: Editorial, Review, Other

23 pages, 8810 KiB  
Article
MiR-155 Negatively Regulates Anti-Viral Innate Responses among HIV-Infected Progressors
by Puja Pawar, Jyotsna Gokavi, Shilpa Wakhare, Rajani Bagul, Ujjwala Ghule, Ishrat Khan, Varada Ganu, Anupam Mukherjee, Ashwini Shete, Amrita Rao and Vandana Saxena
Viruses 2023, 15(11), 2206; https://doi.org/10.3390/v15112206 - 01 Nov 2023
Cited by 1 | Viewed by 1091
Abstract
HIV infection impairs host immunity, leading to progressive disease. An anti-retroviral treatment efficiently controls viremia but cannot completely restore the immune dysfunction in HIV-infected individuals. Both host and viral factors determine the rate of disease progression. Among the host factors, innate immunity plays [...] Read more.
HIV infection impairs host immunity, leading to progressive disease. An anti-retroviral treatment efficiently controls viremia but cannot completely restore the immune dysfunction in HIV-infected individuals. Both host and viral factors determine the rate of disease progression. Among the host factors, innate immunity plays a critical role; however, the mechanism(s) associated with dysfunctional innate responses are poorly understood among HIV disease progressors, which was investigated here. The gene expression profiles of TLRs and innate cytokines in HIV-infected (LTNPs and progressors) and HIV-uninfected individuals were examined. Since the progressors showed a dysregulated TLR-mediated innate response, we investigated the role of TLR agonists in restoring the innate functions of the progressors. The stimulation of PBMCs with TLR3 agonist-poly:(I:C), TLR7 agonist-GS-9620 and TLR9 agonist-ODN 2216 resulted in an increased expression of IFN-α, IFN-β and IL-6. Interestingly, the expression of IFITM3, BST-2, IFITM-3, IFI-16 was also increased upon stimulation with TLR3 and TLR7 agonists, respectively. To further understand the molecular mechanism involved, the role of miR-155 was explored. Increased miR-155 expression was noted among the progressors. MiR-155 inhibition upregulated the expression of TLR3, NF-κB, IRF-3, TNF-α and the APOBEC-3G, IFITM-3, IFI-16 and BST-2 genes in the PBMCs of the progressors. To conclude, miR-155 negatively regulates TLR-mediated cytokines as wel l as the expression of host restriction factors, which play an important role in mounting anti-HIV responses; hence, targeting miR-155 might be helpful in devising strategic approaches towards alleviating HIV disease progression. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

17 pages, 41125 KiB  
Article
Nipah Virus Impairs Autocrine IFN Signaling by Sequestering STAT1 and STAT2 into Inclusion Bodies
by Nico Becker and Andrea Maisner
Viruses 2023, 15(2), 554; https://doi.org/10.3390/v15020554 - 17 Feb 2023
Cited by 2 | Viewed by 2035
Abstract
Nipah virus (NiV) is an emerging zoonotic paramyxovirus that causes fatal infections in humans. As with most disease-causing viruses, the pathogenic potential of NiV is linked to its ability to block antiviral responses, e.g., by antagonizing IFN signaling through blocking STAT proteins. One [...] Read more.
Nipah virus (NiV) is an emerging zoonotic paramyxovirus that causes fatal infections in humans. As with most disease-causing viruses, the pathogenic potential of NiV is linked to its ability to block antiviral responses, e.g., by antagonizing IFN signaling through blocking STAT proteins. One of the STAT1/2-binding proteins of NiV is the phosphoprotein (P), but its functional role in IFN antagonism in a full viral context is not well defined. As NiV P is required for genome replication and specifically accumulates in cytosolic inclusion bodies (IBs) of infected cells, we hypothesized that this compartmentalization might play a role in P-mediated IFN antagonism. Supporting this notion, we show here that NiV can inhibit IFN-dependent antiviral signaling via a NiV P-dependent sequestration of STAT1 and STAT2 into viral IBs. Consequently, the phosphorylation/activation and nuclear translocation of STAT proteins in response to IFN is limited, as indicated by the lack of nuclear pSTAT in NiV-infected cells. Blocking autocrine IFN signaling by sequestering STAT proteins in IBs is a not yet described mechanism by which NiV could block antiviral gene expression and provides the first evidence that cytosolic NiV IBs may play a functional role in IFN antagonism. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

19 pages, 3092 KiB  
Article
HIV-1 Gag Binds the Multi-Aminoacyl-tRNA Synthetase Complex via the EPRS Subunit
by Danni Jin, Yiping Zhu, Heidi L. Schubert, Stephen P. Goff and Karin Musier-Forsyth
Viruses 2023, 15(2), 474; https://doi.org/10.3390/v15020474 - 08 Feb 2023
Cited by 3 | Viewed by 1714
Abstract
Host factor tRNAs facilitate the replication of retroviruses such as human immunodeficiency virus type 1 (HIV-1). HIV-1 uses human tRNALys3 as the primer for reverse transcription, and the assembly of HIV-1 structural protein Gag at the plasma membrane (PM) is regulated by [...] Read more.
Host factor tRNAs facilitate the replication of retroviruses such as human immunodeficiency virus type 1 (HIV-1). HIV-1 uses human tRNALys3 as the primer for reverse transcription, and the assembly of HIV-1 structural protein Gag at the plasma membrane (PM) is regulated by matrix (MA) domain–tRNA interactions. A large, dynamic multi-aminoacyl-tRNA synthetase complex (MSC) exists in the cytosol and consists of eight aminoacyl-tRNA synthetases (ARSs) and three other cellular proteins. Proteomic studies to identify HIV–host interactions have identified the MSC as part of the HIV-1 Gag and MA interactomes. Here, we confirmed that the MA domain of HIV-1 Gag forms a stable complex with the MSC, mapped the primary interaction site to the linker domain of bi-functional human glutamyl-prolyl-tRNA synthetase (EPRS), and showed that the MA–EPRS interaction was RNA dependent. MA mutations that significantly reduced the EPRS interaction reduced viral infectivity and mapped to MA residues that also interact with phosphatidylinositol-(4,5)-bisphosphate. Overexpression of EPRS or EPRS fragments did not affect susceptibility to HIV-1 infection, and knockdown of EPRS reduced both a control reporter gene and HIV-1 protein translation. EPRS knockdown resulted in decreased progeny virion production, but the decrease could not be attributed to selective effects on virus gene expression, and the specific infectivity of the virions remained unchanged. While the precise function of the Gag–EPRS interaction remains uncertain, we discuss possible effects of the interaction on either virus or host activities. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

16 pages, 2088 KiB  
Article
COS-7 and SVGp12 Cellular Models to Study JCPyV Replication and MicroRNA Expression after Infection with Archetypal and Rearranged-NCCR Viral Strains
by Carla Prezioso, Sara Passerini, Dolores Limongi, Anna Teresa Palamara, Ugo Moens and Valeria Pietropaolo
Viruses 2022, 14(9), 2070; https://doi.org/10.3390/v14092070 - 17 Sep 2022
Cited by 5 | Viewed by 1791
Abstract
Since the non-coding control region (NCCR) and microRNA (miRNA) could represent two different and independent modalities of regulating JC polyomavirus (JCPyV) replication at the transcriptional and post-transcriptional levels, the interplay between JC viral load based on NCCR architecture and miRNA levels, following JCPyV [...] Read more.
Since the non-coding control region (NCCR) and microRNA (miRNA) could represent two different and independent modalities of regulating JC polyomavirus (JCPyV) replication at the transcriptional and post-transcriptional levels, the interplay between JC viral load based on NCCR architecture and miRNA levels, following JCPyV infection with archetypal and rearranged (rr)-NCCR JCPyV variants, was explored in COS-7 and SVGp12 cells infected by different JCPyV strains. Specifically, the involvement of JCPyV miRNA in regulating viral replication was investigated for the archetypal CY strain—which is the transmissible form—and for the rearranged MAD-1 strain, which is the first isolated variant from patients with progressive multifocal leukoencephalopathy. The JCPyV DNA viral load was low in cells infected with CY compared with that in MAD-1-infected cells. Productive viral replication was observed in both cell lines. The expression of JCPyV miRNAs was observed from 3 days after viral infection in both cell types, and miR-J1-5p expression was inversely correlated with the JCPyV replication trend. The JCPyV miRNAs in the exosomes present in the supernatants produced by the infected cells could be carried into uninfected cells. Additional investigations of the expression of JCPyV miRNAs and their presence in exosomes are necessary to shed light on their regulatory role during viral reactivation. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

28 pages, 5989 KiB  
Article
Dengue Virus NS4b N-Terminus Disordered Region Interacts with NS3 Helicase C-Terminal Subdomain to Enhance Helicase Activity
by Satyamurthy Kundharapu and Tirumala Kumar Chowdary
Viruses 2022, 14(8), 1712; https://doi.org/10.3390/v14081712 - 03 Aug 2022
Cited by 3 | Viewed by 2582
Abstract
Dengue virus replicates its single-stranded RNA genome in membrane-bound complexes formed on the endoplasmic reticulum, where viral non-structural proteins (NS) and RNA co-localize. The NS proteins interact with one another and with the host proteins. The interaction of the viral helicase and protease, [...] Read more.
Dengue virus replicates its single-stranded RNA genome in membrane-bound complexes formed on the endoplasmic reticulum, where viral non-structural proteins (NS) and RNA co-localize. The NS proteins interact with one another and with the host proteins. The interaction of the viral helicase and protease, NS3, with the RNA-dependent RNA polymerase, NS5, and NS4b proteins is critical for replication. In vitro, NS3 helicase activity is enhanced by interaction with NS4b. We characterized the interaction between NS3 and NS4b and explained a possible mechanism for helicase activity modulation by NS4b. Our bacterial two-hybrid assay results showed that the N-terminal 57 residues region of NS4b is enough to interact with NS3. The molecular docking of the predicted NS4b structure onto the NS3 structure revealed that the N-terminal disordered region of NS4b wraps around the C-terminal subdomain (CTD) of the helicase. Further, NS3 helicase activity is enhanced upon interaction with NS4b. Molecular dynamics simulations on the NS4b-docked NS3 crystal structure and intrinsic tryptophan fluorescence studies suggest that the interaction results in NS3 CTD domain motions. Based on the interpretation of our results in light of the mechanism explained for NS3 helicase, NS4b–NS3 interaction modulating CTD dynamics is a plausible explanation for the helicase activity enhancement. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

14 pages, 1971 KiB  
Article
Human Beta Papillomavirus Type 8 E1 and E2 Proteins Suppress the Activation of the RIG-I-Like Receptor MDA5
by Stephanie Rattay, Martin Hufbauer, Christian Hagen, Bastian Putschli, Christoph Coch, Baki Akgül and Gunther Hartmann
Viruses 2022, 14(7), 1361; https://doi.org/10.3390/v14071361 - 22 Jun 2022
Cited by 7 | Viewed by 1888
Abstract
Persistent infections of the skin with the human papillomavirus of genus beta (β-HPV) in immunocompetent individuals are asymptomatic, but in immunosuppressed patients, β-HPV infections exhibit much higher viral loads on the skin and are associated with an increased risk of skin cancer. Unlike [...] Read more.
Persistent infections of the skin with the human papillomavirus of genus beta (β-HPV) in immunocompetent individuals are asymptomatic, but in immunosuppressed patients, β-HPV infections exhibit much higher viral loads on the skin and are associated with an increased risk of skin cancer. Unlike with HPV16, a high-risk α-HPV, the impact of β-HPV early genes on the innate immune sensing of viral nucleic acids has not been studied. Here, we used primary skin keratinocytes and U2OS cells expressing HPV8 or distinct HPV8 early genes and well-defined ligands of the nucleic-acid-sensing receptors RIG-I, MDA5, TLR3, and STING to analyze a potential functional interaction. We found that primary skin keratinocytes and U2OS cells expressed RIG-I, MDA5, TLR3, and STING, but not TLR7, TLR8, or TLR9. While HPV16-E6 downregulated the expression of RIG-I, MDA5, TLR3, and STING and, in conjunction with HPV16-E7, effectively suppressed type I IFN in response to MDA5 activation, the presence of HPV8 early genes showed little effect on the expression of these immune receptors, except for HPV8-E2, which was associated with an elevated expression of TLR3. Nevertheless, whole HPV8 genome expression, as well as the selective expression of HPV8-E1 or HPV8-E2, was found to suppress MDA5-induced type I IFN and the proinflammatory cytokine IL-6. Furthermore, RNA isolated from HPV8-E2 expressing primary human keratinocytes, but not control cells, stimulated a type I IFN response in peripheral blood mononuclear cells, indicating that the expression of HPV8-E2 in keratinocytes leads to the formation of stimulatory RNA ligands that require the active suppression of immune recognition. These results identify HPV8-E1 and HPV8-E2 as viral proteins that are responsible for the immune escape of β-HPV from the innate recognition of viral nucleic acids, a mechanism that may be necessary for establishing persistent β-HPV infections. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research, Other

11 pages, 1185 KiB  
Review
Hepatitis Delta Virus–Host Protein Interactions: From Entry to Egress
by Susannah Stephenson-Tsoris and T. Jake Liang
Viruses 2023, 15(7), 1530; https://doi.org/10.3390/v15071530 - 11 Jul 2023
Cited by 1 | Viewed by 1399
Abstract
Hepatitis delta virus (HDV) is the smallest known human virus and causes the most severe form of human viral hepatitis, yet it is still not fully understood how the virus replicates and how it interacts with many host proteins during replication. This review [...] Read more.
Hepatitis delta virus (HDV) is the smallest known human virus and causes the most severe form of human viral hepatitis, yet it is still not fully understood how the virus replicates and how it interacts with many host proteins during replication. This review aims to provide a systematic review of all the host factors currently known to interact with HDV and their mechanistic involvement in all steps of the HDV replication cycle. Finally, we discuss implications for therapeutic development based on our current knowledge of HDV–host protein interactions. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

22 pages, 4655 KiB  
Review
miRNAs in Herpesvirus Infection: Powerful Regulators in Small Packages
by Debashree Dass, Kishore Dhotre, Muskan Chakraborty, Anushka Nath, Anwesha Banerjee, Parikshit Bagchi and Anupam Mukherjee
Viruses 2023, 15(2), 429; https://doi.org/10.3390/v15020429 - 03 Feb 2023
Cited by 7 | Viewed by 2220
Abstract
microRNAs are a class of small, single-stranded, noncoding RNAs that regulate gene expression. They can be significantly dysregulated upon exposure to any infection, serving as important biomarkers and therapeutic targets. Numerous human DNA viruses, along with several herpesviruses, have been found to encode [...] Read more.
microRNAs are a class of small, single-stranded, noncoding RNAs that regulate gene expression. They can be significantly dysregulated upon exposure to any infection, serving as important biomarkers and therapeutic targets. Numerous human DNA viruses, along with several herpesviruses, have been found to encode and express functional viral microRNAs known as vmiRNAs, which can play a vital role in host–pathogen interactions by controlling the viral life cycle and altering host biological pathways. Viruses have also adopted a variety of strategies to prevent being targeted by cellular miRNAs. Cellular miRNAs can act as anti- or proviral components, and their dysregulation occurs during a wide range of infections, including herpesvirus infection. This demonstrates the significance of miRNAs in host herpesvirus infection. The current state of knowledge regarding microRNAs and their role in the different stages of herpes virus infection are discussed in this review. It also delineates the therapeutic and biomarker potential of these microRNAs in future research directions. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

18 pages, 1624 KiB  
Review
Cellular Sensors and Viral Countermeasures: A Molecular Arms Race between Host and SARS-CoV-2
by Haoran Sun, Jasper Fuk-Woo Chan and Shuofeng Yuan
Viruses 2023, 15(2), 352; https://doi.org/10.3390/v15020352 - 26 Jan 2023
Cited by 2 | Viewed by 1904
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19) pandemic that has caused disastrous effects on the society and human health globally. SARS-CoV-2 is a sarbecovirus in the Coronaviridae family with a positive-sense single-stranded RNA [...] Read more.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the coronavirus disease 2019 (COVID-19) pandemic that has caused disastrous effects on the society and human health globally. SARS-CoV-2 is a sarbecovirus in the Coronaviridae family with a positive-sense single-stranded RNA genome. It mainly replicates in the cytoplasm and viral components including RNAs and proteins can be sensed by pattern recognition receptors including toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and NOD-like receptors (NLRs) that regulate the host innate and adaptive immune responses. On the other hand, the SARS-CoV-2 genome encodes multiple proteins that can antagonize the host immune response to facilitate viral replication. In this review, we discuss the current knowledge on host sensors and viral countermeasures against host innate immune response to provide insights on virus–host interactions and novel approaches to modulate host inflammation and antiviral responses. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

16 pages, 1911 KiB  
Review
Flavivirus–Host Interaction Landscape Visualized through Genome-Wide CRISPR Screens
by Aditi Kanojia, Mansi Sharma, Rishad Shiraz and Shashank Tripathi
Viruses 2022, 14(10), 2164; https://doi.org/10.3390/v14102164 - 30 Sep 2022
Cited by 5 | Viewed by 3121
Abstract
Flaviviruses comprise several important human pathogens which cause significant morbidity and mortality worldwide. Like any other virus, they are obligate intracellular parasites. Therefore, studying the host cellular factors that promote or restrict their replication and pathogenesis becomes vital. Since inhibiting the host dependency [...] Read more.
Flaviviruses comprise several important human pathogens which cause significant morbidity and mortality worldwide. Like any other virus, they are obligate intracellular parasites. Therefore, studying the host cellular factors that promote or restrict their replication and pathogenesis becomes vital. Since inhibiting the host dependency factors or activating the host restriction factors can suppress the viral replication and propagation in the cell, identifying them reveals potential targets for antiviral therapeutics. Clustered regularly interspaced short palindromic repeats (CRISPR) technology has provided an effective means of producing customizable genetic modifications and performing forward genetic screens in a broad spectrum of cell types and organisms. The ease, rapidity, and high reproducibility of CRISPR technology have made it an excellent tool for carrying out genome-wide screens to identify and characterize viral host dependency factors systematically. Here, we review the insights from various Genome-wide CRISPR screens that have advanced our understanding of Flavivirus-Host interactions. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

18 pages, 2490 KiB  
Review
Complexities of JC Polyomavirus Receptor-Dependent and -Independent Mechanisms of Infection
by Jenna Morris-Love and Walter J. Atwood
Viruses 2022, 14(6), 1130; https://doi.org/10.3390/v14061130 - 24 May 2022
Cited by 7 | Viewed by 2897
Abstract
JC polyomavirus (JCPyV) is a small non-enveloped virus that establishes lifelong, persistent infection in most of the adult population. Immune-competent patients are generally asymptomatic, but immune-compromised and immune-suppressed patients are at risk for the neurodegenerative disease progressive multifocal leukoencephalopathy (PML). Studies with purified [...] Read more.
JC polyomavirus (JCPyV) is a small non-enveloped virus that establishes lifelong, persistent infection in most of the adult population. Immune-competent patients are generally asymptomatic, but immune-compromised and immune-suppressed patients are at risk for the neurodegenerative disease progressive multifocal leukoencephalopathy (PML). Studies with purified JCPyV found it undergoes receptor-dependent infectious entry requiring both lactoseries tetrasaccharide C (LSTc) attachment and 5-hydroxytryptamine type 2 entry receptors. Subsequent work discovered the major targets of JCPyV infection in the central nervous system (oligodendrocytes and astrocytes) do not express the required attachment receptor at detectable levels, virus could not bind these cells in tissue sections, and viral quasi-species harboring recurrent mutations in the binding pocket for attachment. While several research groups found evidence JCPyV can use novel receptors for infection, it was also discovered that extracellular vesicles (EVs) can mediate receptor independent JCPyV infection. Recent work also found JCPyV associated EVs include both exosomes and secretory autophagosomes. EVs effectively present a means of immune evasion and increased tissue tropism that complicates viral studies and anti-viral therapeutics. This review focuses on JCPyV infection mechanisms and EV associated and outlines key areas of study necessary to understand the interplay between virus and extracellular vesicles. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

Other

4 pages, 199 KiB  
Reply
Reply to Henriksen, S.; Rinaldo, C.H. Should SVGp12 Be Used for JC Polyomavirus Studies? Comment on “Prezioso et al. COS-7 and SVGp12 Cellular Models to Study JCPyV Replication and MicroRNA Expression after Infection with Archetypal and Rearranged-NCCR Viral Strains. Viruses 2022, 14, 2070”
by Carla Prezioso, Ugo Moens and Valeria Pietropaolo
Viruses 2023, 15(1), 93; https://doi.org/10.3390/v15010093 - 29 Dec 2022
Cited by 1 | Viewed by 1318
Abstract
In relation to the comment by Henriksen and Rinaldo, the authors intend to emphasize that before every experiment with SVGp12 cells they routinely test the cells for the absence of BKPyV contamination. The scientists can state that the SVGp12 cells used in their [...] Read more.
In relation to the comment by Henriksen and Rinaldo, the authors intend to emphasize that before every experiment with SVGp12 cells they routinely test the cells for the absence of BKPyV contamination. The scientists can state that the SVGp12 cells used in their laboratory were not infected by BKPyV and that their results were also validated on the COS-7 cell line, which is permissive for JCPyV infection. Therefore, the overall findings of the study and its conclusions remain authentic. The authors recommend the necessity of carefully testing SVGp12 cells for BKPyV infection before use or, alternatively, in case of a first purchase; moreover, it is possible to choose different cell lines to avoid running into this unpleasant situation. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
3 pages, 530 KiB  
Comment
Should SVGp12 Be Used for JC Polyomavirus Studies? Comment on Prezioso et al. COS-7 and SVGp12 Cellular Models to Study JCPyV Replication and MicroRNA Expression after Infection with Archetypal and Rearranged-NCCR Viral Strains. Viruses 2022, 14, 2070
by Stian Henriksen and Christine Hanssen Rinaldo
Viruses 2023, 15(1), 89; https://doi.org/10.3390/v15010089 - 29 Dec 2022
Cited by 2 | Viewed by 855
Abstract
A recent paper in Viruses investigates the impact of the JC polyomavirus (JCPyV) microRNA on the replication of different JCPyV strains. Unfortunately, one of the cell lines used, the human fetal glial cell line SVGp12, is productively infected by the closely related BK [...] Read more.
A recent paper in Viruses investigates the impact of the JC polyomavirus (JCPyV) microRNA on the replication of different JCPyV strains. Unfortunately, one of the cell lines used, the human fetal glial cell line SVGp12, is productively infected by the closely related BK polyomavirus (BKPyV), which may confound results. Scientists need to take this into account and the potential pitfalls. Full article
(This article belongs to the Special Issue Host Cell–Virus Interaction 2.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-14
Back to TopTop