scholarly journals Activation of E2F-dependent transcription by the mouse cytomegalovirus M117 protein affects the viral host range

2018 ◽  
Vol 14 (12) ◽  
pp. e1007481 ◽  
Author(s):  
Eléonore Ostermann ◽  
Stefan Loroch ◽  
Zhikang Qian ◽  
Albert Sickmann ◽  
Lüder Wiebusch ◽  
...  
Keyword(s):  
Host Range ◽  
Mouse Cytomegalovirus ◽  
Viral Host Range

scholarly journals Viral Host Range database, an online tool for recording, analyzing and disseminating virus-host interactions

2021 ◽  
Author(s):  
Quentin Lamy-Besnier ◽  
Bryan Brancotte ◽  
Hervé Ménager ◽  
Laurent Debarbieux
Keyword(s):  
Host Range ◽  
Source Code ◽  
Range Data ◽  
Web Based ◽  
Online Tool ◽  
Experimental Host ◽  
Living World ◽  
Host Interactions ◽  
Experimental Host Range ◽  
Viral Host Range

Abstract Motivation Viruses are ubiquitous in the living world, and their ability to infect more than one host defines their host range. However, information about which virus infects which host, and about which host is infected by which virus, is not readily available. Results We developed a web-based tool called the Viral Host Range database to record, analyze and disseminate experimental host range data for viruses infecting archaea, bacteria and eukaryotes. Availability The ViralHostRangeDB application is available from https://viralhostrangedb.pasteur.cloud. Its source code is freely available from the Gitlab hub of Institut Pasteur (https://gitlab.pasteur.fr/hub/viralhostrangedb).

scholarly journals A Poxvirus Host Range Protein, CP77, Binds to a Cellular Protein, HMG20A, and Regulates Its Dissociation from the Vaccinia Virus Genome in CHO-K1 Cells

2006 ◽  
Vol 80 (15) ◽  
pp. 7714-7728 ◽  
Author(s):  
Jye-Chian Hsiao ◽  
Chien-Chiang Chao ◽  
Ming-Jer Young ◽  
Yu-Tai Chang ◽  
Er-Chieh Cho ◽  
...  
Keyword(s):  
Amino Acids ◽  
Vaccinia Virus ◽  
Host Range ◽  
Viral Genome ◽  
Cellular Protein ◽  
Deletion Mapping ◽  
Viral Dna ◽  
Virus Growth ◽  
Range Function ◽  
Viral Host Range

ABSTRACT Vaccinia virus does not grow in Chinese hamster ovary (CHO-K1) cells in the absence of a viral host range factor, cowpox protein CP77. In this study, CP77 was fused to the C terminus of green fluorescence protein (GFP-CP77) and a series of nested deletion mutants of GFP-CP77 was constructed for insertion into a vaccinia virus host range mutant, VV-hr, and expressed from a viral early promoter. Deletion mapping analyses demonstrated that the N-terminal 352 amino acids of CP77 were sufficient to support vaccinia virus growth in CHO-K1 cells, whereas the C-terminal residues 353 to 668 were dispensable. In yeast two-hybrid analyses, CP77 bound to a cellular protein, HMG20A, and GST pulldown analyses showed that residues 1 to 234 of CP77 were sufficient for this interaction. After VV-hr virus infection of CHO-K1 cells, HMG20A was translocated from the nucleus to viral factories and bound to the viral genome via the HMG box region. In control VV-hr-infected CHO-K1 cells, binding of HMG20A to the viral genome persisted from 2 to 8 h postinfection (h p.i.); in contrast, when CP77 was expressed, the association of HMG20A with viral genome was transient, with little HMG20A remaining bound at 8 h p.i. This indicates that dissociation of HMG20A from viral factories correlates well with CP77 host range activity in CHO-K1 cells. Finally, in cells expressing a CP77 deletion protein (amino acids 277 to 668) or a ΔANK5 mutant that did not support vaccinia virus growth and did not contain the HMG20A binding site, HMG20A remained bound to viral DNA, demonstrating that the binding of CP77 to HMG20A is essential for its host range function. In summary, our data revealed that a novel cellular protein, HMG20A, the dissociation of which from viral DNA is regulated by CP77, providing the first cellular target regulated by viral host range CP77 protein.

scholarly journals Mutational Analysis of Aminopeptidase N, a Receptor for Several Group 1 Coronaviruses, Identifies Key Determinants of Viral Host Range

2006 ◽  
Vol 81 (3) ◽  
pp. 1261-1273 ◽  
Author(s):  
Sonia M. Tusell ◽  
Stephanie A. Schittone ◽  
Kathryn V. Holmes
Keyword(s):  
Host Range ◽  
Mutational Analysis ◽  
Aminopeptidase N ◽  
Receptor Activity ◽  
Specific Amino Acid ◽  
Transmissible Gastroenteritis ◽  
Species Specific ◽  
Viral Host Range ◽  
Feline Coronavirus ◽  
Group 1

ABSTRACT Feline coronavirus (FCoV), porcine transmissible gastroenteritis coronavirus (TGEV), canine coronavirus (CCoV), and human coronavirus HCoV-229E, which belong to the group 1 coronavirus, use aminopeptidase N (APN) of their natural host and feline APN (fAPN) as receptors. Using mouse-feline APN chimeras, we identified three small, discontinuous regions, amino acids (aa) 288 to 290, aa 732 to 746 (called R1), and aa 764 to 788 (called R2) in fAPN that determined the host ranges of these coronaviruses. Blockade of infection with anti-fAPN monoclonal antibody RG4 suggested that these three regions lie close together on the fAPN surface. Different residues in fAPN were required for infection with each coronavirus. HCoV-229E infection was blocked by an N-glycosylation sequon present between aa 288 to 290 in murine APN. TGEV required R1 of fAPN, while FCoV and CCoV required both R1 and R2 for entry. N740 and T742 in fAPN and the homologous R741 in human APN (hAPN) were key determinants of host range for FCoV, TGEV, and CCoV. Residue N740 in fAPN was essential only for CCoV receptor activity. A conservative T742V substitution or a T742R substitution in fAPN destroyed receptor activity for the pig, dog, and cat coronaviruses, while a T742S substitution retained these receptor activities. Thus, the hydroxyl on T742 is required for the coronavirus receptor activity of fAPN. In hAPN an R741T substitution caused a gain of receptor activity for TGEV but not for FCoV or CCoV. Therefore, entry and host range of these group 1 coronaviruses depend on the ability of the viral spike glycoproteins to recognize small, species-specific amino acid differences in the APN proteins of different species.

scholarly journals The B1.351 and P.1 variants extend SARS-CoV-2 host range to mice

2021 ◽  
Author(s):  
Xavier Montagutelli ◽  
Matthieu Prot ◽  
Laurine Levillayer ◽  
Eduard Baquero Salazar ◽  
Gregory Jouvion ◽  
...  
Keyword(s):  
Host Range ◽  
Immune Escape ◽  
Experimental Models ◽  
Species Barrier ◽  
Angiotensin Converting Enzyme 2 ◽  
Host Shifts ◽  
Receptor Recognition ◽  
Novel Host ◽  
Viral Host Range ◽  
Common Laboratory

Receptor recognition is a major determinant of viral host range, as well as infectivity and pathogenesis. Emergences have been associated with serendipitous events of adaptation upon encounters with a novel host, and the high mutation rate of RNA viruses has been proposed to explain their frequent host shifts. SARS-CoV-2 extensive circulation in humans has been associated with the emergence of variants, including variants of concern (VOCs) with diverse mutations in the spike and increased transmissibility or immune escape. Here we show that unlike the initial virus, VOCs are able to infect common laboratory mice, replicating to high titers in the lungs. This host range expansion is explained in part by the acquisition of changes at key positions of the receptor binding domain that enable binding to the mouse angiotensin-converting enzyme 2 (ACE2) cellular receptor, although differences between viral lineages suggest that other factors are involved in the capacity of SARS-CoV-2 VOCs to infect mice. This abrogation of the species barrier raises the possibility of wild rodent secondary reservoirs and provides new experimental models to study disease pathophysiology and countermeasures.

scholarly journals Characterization of a bacteriophage from urban sewage obtained with the bacterium Staphylococcus aureus

2020 ◽  
Vol 10 (1) ◽  
pp. 20-24
Author(s):  
Anderson Luiz Pena da Costa ◽  
Antonio Carlos Freitas Souza ◽  
Rafael Lima Resque
Keyword(s):  
Host Range ◽  
Pathogenic Bacteria ◽  
Fragment Length Polymorphism ◽  
Bacterial Species ◽  
Pharmaceutical Product ◽  
Urban Sewage ◽  
Viral Host Range ◽  
Significant Attention

Bacteriophages are viruses of bacteria that have received significant attention in the last decades due to their potential as an alternative to the antibiotics, as well as their applicability in the selective control of bacterial species harmful to food. In this context, this work reports the partial results of a viral filtrate named P4CSa that was obtained with the bacterium Staphylococcus aureusand characterized by the viral host range and the restriction fragment length polymorphism technique. The results indicate that the phage P4CSa probably belongs to the order Caudovirales, it presents a polyvalent host range, and it can be preserved for the long term in the form of filtrated lysates stored at 4°C, suggesting that the phage P4CSa may have the potential for the development of a pharmaceutical product indicated for the biocontrol of pathogenic bacteria. Stamford Journal of Microbiology, Vol.10 (1) 2020: 20-24

scholarly journals Both Bipartite Geminivirus Movement Proteins Define Viral Host Range, but Only BL1 Determines Viral Pathogenicity

Virology ◽  
1995 ◽  
Vol 207 (1) ◽  
pp. 191-204 ◽  
Author(s):  
David J. Ingham ◽  
Erica Pascal ◽  
Sondra G. Lazarowitz
Keyword(s):  
Host Range ◽  
Movement Proteins ◽  
Viral Host Range

scholarly journals Identification of Restriction Factors by Human Genome-Wide RNA Interference Screening of Viral Host Range Mutants Exemplified by Discovery of SAMD9 and WDR6 as Inhibitors of the Vaccinia Virus K1L−C7L− Mutant

mBio ◽  
2015 ◽  
Vol 6 (4) ◽  
Author(s):  
Gilad Sivan ◽  
Pinar Ormanoglu ◽  
Eugen C. Buehler ◽  
Scott E. Martin ◽  
Bernard Moss
Keyword(s):  
Green Fluorescent Protein ◽  
Rna Interference ◽  
Vaccinia Virus ◽  
Host Range ◽  
Human Genome ◽  
Fluorescent Protein ◽  
Restriction Factors ◽  
Genome Wide ◽  
Green Fluorescent ◽  
Viral Host Range

ABSTRACTRNA interference (RNAi) screens intended to identify host factors that restrict virus replication may fail if the virus already counteracts host defense mechanisms. To overcome this limitation, we are investigating the use of viral host range mutants that exhibit impaired replication in nonpermissive cells. A vaccinia virus (VACV) mutant with a deletion of both the C7L and K1L genes, K1L−C7L−, which abrogates replication in human cells at a step prior to late gene expression, was chosen for this strategy. We carried out a human genome-wide small interfering RNA (siRNA) screen in HeLa cells infected with a VACV K1L−C7L−mutant that expresses the green fluorescent protein regulated by a late promoter. This positive-selection screen had remarkably low background levels and resulted in the identification of a few cellular genes, notably SAMD9 and WDR6, from approximately 20,000 tested that dramatically enhanced green fluorescent protein expression. Replication of the mutant virus was enabled by multiple siRNAs to SAMD9 or WDR6. Moreover, SAMD9 and WDR6 clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 knockout HeLa cell lines were permissive for replication of the K1L−C7L−mutant, in agreement with the siRNA data. Expression of exogenous SAMD9 or interferon regulatory factor 1 restricted replication of the K1L−C7L−mutant in the SAMD9−/−cells. Independent interactions of SAMD9 with the K1 and C7 proteins were suggested by immunoprecipitation. Knockout of WDR6 did not reduce the levels of SAMD9 and interactions of WDR6 with SAMD9, C7, and K1 proteins were not detected, suggesting that these restriction factors act independently but possibly in the same innate defense pathway.IMPORTANCEThe coevolution of microbial pathogens with cells has led to an arms race in which the invader and host continuously struggle to gain the advantage. For this reason, traditional siRNA screens may fail to uncover important immune mechanisms if the pathogens have already developed effective responses. However, host-restricted viral mutants have lost one or more defense genes needed for their replication in nonpermissive cells. By screening human genome libraries of short RNAs that inhibit the expression of individual host genes in nonpermissive cells, we identified SAMD9 and WDR6 as major restriction factors that prevented replication of a vaccinia virus mutant and suggest that host range screening can be generally useful for the investigation of host-pathogen interactions.

Expansion of Viral Host Range through Complementation and Recombination in Transgenic Plants

1993 ◽  
Vol 5 (11) ◽  
pp. 1669 ◽  
Author(s):  
James E. Schoelz ◽  
William M. Wintermantel
Keyword(s):  
Transgenic Plants ◽  
Host Range ◽  
Viral Host Range
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