Coxsackieviral proteins functionally recognize the polioviral cloverleaf structure of the 5′-NTR of a chimeric enterovirus RNA: influence of species-specific host cell factors on virus growth

1995 ◽  
Vol 39 (2-3) ◽  
pp. 87-103 ◽  
Author(s):  
Roland Zell ◽  
Karin Klingel ◽  
Martina Sauter ◽  
Ulrike Fortmüller ◽  
Reinhard Kandolf
Keyword(s):  
Host Cell ◽  
Virus Growth ◽  
Specific Host ◽  
Host Cell Factors ◽  
Species Specific ◽  
Cloverleaf Structure

scholarly journals A Stochastic Model for Virus Growth in a Cell Population

2014 ◽  
Vol 51 (3) ◽  
pp. 599-612 ◽  
Author(s):  
J. E. Björnberg ◽  
T. Britton ◽  
E. I. Broman ◽  
E. Natan
Keyword(s):  
Stochastic Model ◽  
Host Cell ◽  
Cell Population ◽  
Branching Process ◽  
Virus Population ◽  
Virus Growth ◽  
Optimal Balance ◽  
Large Numbers ◽  
A Cell

In this work we introduce a stochastic model for the spread of a virus in a cell population where the virus has two ways of spreading: either by allowing its host cell to live and duplicate, or by multiplying in large numbers within the host cell, causing the host cell to burst and thereby let the virus enter new uninfected cells. The model is a kind of interacting Markov branching process. We focus in particular on the probability that the virus population survives and how this depends on a certain parameter λ which quantifies the ‘aggressiveness’ of the virus. Our main goal is to determine the optimal balance between aggressive growth and long-term success. Our analysis shows that the optimal strategy of the virus (in terms of survival) is obtained when the virus has no effect on the host cell's life cycle, corresponding to λ = 0. This is in agreement with experimental data about real viruses.

scholarly journals Identification of host cell factors common to both mosquito and human cells in response to Dengue virus infection

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Subrat Narayan Rout ◽  
Kevin Ramkissoon ◽  
David Anderson ◽  
Joseph Perrone ◽  
Rajeev Vaidyanathan ◽  
...  
Keyword(s):  
Virus Infection ◽  
Dengue Virus ◽  
Host Cell ◽  
Human Cells ◽  
Dengue Virus Infection ◽  
Host Cell Factors

scholarly journals Heat-Shock Protein 90 Controls the Expression of Cell-Cycle Genes by Stabilizing Metazoan-Specific Host-Cell Factor HCFC1

Cell Reports ◽  
2019 ◽  
Vol 29 (6) ◽  
pp. 1645-1659.e9 ◽  
Author(s):  
Aneliya Antonova ◽  
Barbara Hummel ◽  
Ashkan Khavaran ◽  
Desiree M. Redhaber ◽  
Fernando Aprile-Garcia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Host Cell ◽  
Heat Shock Protein 90 ◽  
Cell Cycle Genes ◽  
Specific Host ◽  
Host Cell Factor

scholarly journals User-Friendly Reverse Genetics System for Modification of the Right End of Fowl Adenovirus 4 Genome

Viruses ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 301
Author(s):  
Bingyu Yan ◽  
Xiaohui Zou ◽  
Xinglong Liu ◽  
Jiaming Zhao ◽  
Wenfeng Zhang ◽  
...  
Keyword(s):  
Reverse Genetics ◽  
Economic Losses ◽  
Virus Growth ◽  
Recombinant Viruses ◽  
Fowl Adenovirus ◽  
Viral Genes ◽  
Lmh Cells ◽  
Species Specific ◽  
The Right ◽  
User Friendly

A novel fowl adenovirus 4 (FAdV-4) has caused significant economic losses to the poultry industry in China since 2015. We established an easy-to-use reverse genetics system for modification of the whole right and partial left ends of the novel FAdV-4 genome, which worked through cell-free reactions of restriction digestion and Gibson assembly. Three recombinant viruses were constructed to test the assumption that species-specific viral genes of ORF4 and ORF19A might be responsible for the enhanced virulence: viral genes of ORF1, ORF1b and ORF2 were replaced with GFP to generate FAdV4-GFP, ORF4 was replaced with mCherry in FAdV4-GFP to generate FAdV4-GX4C, and ORF19A was deleted in FAdV4-GFP to generate FAdV4-CX19A. Deletion of ORF4 made FAdV4-GX4C form smaller plaques while ORF19A deletion made FAdV4-CX19A form larger ones on chicken LMH cells. Coding sequence (CDS) replacement with reporter mCherry demonstrated that ORF4 had a weak promoter. Survival analysis showed that FAdV4-CX19A-infected chicken embryos survived one more day than FAdV4-GFP- or FAdV4-GX4C-infected ones. The results illustrated that ORF4 and ORF19A were non-essential genes for FAdV-4 replication although deletion of either gene influenced virus growth. This work would help function study of genes on the right end of FAdV-4 genome and facilitate development of attenuated vaccines.

scholarly journals Transcytosis of Listeria monocytogenes across the intestinal barrier upon specific targeting of goblet cell accessible E-cadherin

2011 ◽  
Vol 208 (11) ◽  
pp. 2263-2277 ◽  
Author(s):  
Georgios Nikitas ◽  
Chantal Deschamps ◽  
Olivier Disson ◽  
Théodora Niault ◽  
Pascale Cossart ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Intestinal Epithelium ◽  
Foodborne Pathogen ◽  
Intestinal Barrier ◽  
Systemic Infection ◽  
Surface Protein ◽  
Intestinal Lumen ◽  
Specific Host ◽  
Species Specific ◽  
E Cadherin

Listeria monocytogenes (Lm) is a foodborne pathogen that crosses the intestinal barrier upon interaction between its surface protein InlA and its species-specific host receptor E-cadherin (Ecad). Ecad, the key constituent of adherens junctions, is typically situated below tight junctions and therefore considered inaccessible from the intestinal lumen. In this study, we investigated how Lm specifically targets its receptor on intestinal villi and crosses the intestinal epithelium to disseminate systemically. We demonstrate that Ecad is luminally accessible around mucus-expelling goblet cells (GCs), around extruding enterocytes at the tip and lateral sides of villi, and in villus epithelial folds. We show that upon preferential adherence to accessible Ecad on GCs, Lm is internalized, rapidly transcytosed across the intestinal epithelium, and released in the lamina propria by exocytosis from where it disseminates systemically. Together, these results show that Lm exploits intrinsic tissue heterogeneity to access its receptor and reveal transcytosis as a novel and unanticipated pathway that is hijacked by Lm to breach the intestinal epithelium and cause systemic infection.

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