scholarly journals Of mice and men: A small animal model of hepatitis C virus replication

Hepatology ◽  
2002 ◽  
Vol 35 (3) ◽  
pp. 722-724 ◽  
Author(s):  
Volker Brass ◽  
Hubert E. Blum ◽  
Darius Moradpour
Keyword(s):  
Animal Model ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Replication ◽  
Small Animal ◽  
Small Animal Model ◽  
Of Mice And Men

scholarly journals Antisense Oligonucleotide Inhibition of Hepatitis C Virus (HCV) Gene Expression in Livers of Mice Infected with an HCV-Vaccinia Virus Recombinant

1999 ◽  
Vol 43 (2) ◽  
pp. 347-353 ◽  
Author(s):  
Hong Zhang ◽  
Ronnie Hanecak ◽  
Vickie Brown-Driver ◽  
Raana Azad ◽  
Boyd Conklin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Animal Model ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Vaccinia Virus ◽  
Antisense Oligonucleotides ◽  
Small Animal ◽  
Initiation Codon ◽  
Small Animal Model ◽  
Recombinant Vaccinia

ABSTRACT Hepatitis C virus (HCV) is the major cause of non-A, non-B hepatitis worldwide. Current treatments are not curative for most infected individuals, and there is an urgent need for both novel therapeutic agents and small-animal models which can be used to evaluate candidate drugs. A small-animal model of HCV gene expression was developed with recombinant vaccinia virus vectors. VHCV-IRES (internal ribosome entry site) is a recombinant vaccinia viral vector containing the HCV 5′ nontranslated region (5′-NTR) and a portion of the HCV core coding region fused to the firefly luciferase gene. Intraperitoneal injection of VHCV-IRES produced high levels of luciferase activity in the livers of BALB/c mice. Antisense oligonucleotides complementary to the HCV 5′-NTR and translation initiation codon regions were then evaluated for their effects on the expression of these target HCV sequences in BALB/c mice infected with the vaccinia virus vector. Treatment of VHCV-IRES-infected mice with 20-base phosphorothioate oligonucleotides complementary to the sequence surrounding the HCV initiation codon (nucleotides 330 to 349) specifically reduced luciferase expression in the livers in a dose-dependent manner. Inhibition of HCV reporter gene expression in this small-animal model suggests that antisense oligonucleotides may provide a novel therapy for treatment of chronic HCV infection.

scholarly journals Viral Persistence and Chronicity in Hepatitis C Virus Infection: Role of T-Cell Apoptosis, Senescence and Exhaustion

2018 ◽  
Author(s):  
Muttiah Barathan ◽  
Rosmawati Mohamed ◽  
Yean K. Yong ◽  
Meganathan Kannan ◽  
Jamuna Vadivelu ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Small Animal ◽  
Viral Escape ◽  
Hepatitis C Virus Infection ◽  
Small Animal Model ◽  
T Cell Apoptosis ◽  
Early Phases

Hepatitis C virus (HCV) represents a challenging global health threat in ~200 million infected individuals. Clinical data suggests that only ~10-15% of acutely HCV-infected individuals will achieve spontaneous viral clearance despite exuberant virus-specific immune responses, which is largely attributed to difficulties in recognizing the pathognomonic symptoms during the initial stages of exposure to the virus. Given the paucity of a suitable small animal model, it is also equally challenging to study the early phases of viral establishment. Further, the host factors contributing to HCV chronicity in a vast majority of acutely HCV-infected individuals largely remain unexplored. The last few years have witnessed a surge in studies showing that HCV adopts a myriad mechanisms to disconcert virus-specific immune responses in the host to establish persistence that includes, but not limited to viral escape mutations, viral growth at privileged sites, and antagonism. Here, we discussed a few hitherto poorly explained mechanisms employed by HCV that are believed to lead to chronicity in infected individuals. A better understanding of these mechanisms would aid the design of improved therapeutic targets against viral establishment in susceptible individuals.

A long-awaited small animal model for hepatitis C

2002 ◽  
Vol 36 (3) ◽  
pp. 447-449
Author(s):  
Chandan Guha ◽  
Jayanta Roy Chowdhury
Keyword(s):  
Animal Model ◽  
Hepatitis C ◽  
Small Animal ◽  
Small Animal Model

scholarly journals Towards a small animal model for hepatitis C

EMBO Reports ◽  
2009 ◽  
Vol 10 (11) ◽  
pp. 1220-1227 ◽  
Author(s):  
Alexander Ploss ◽  
Charles M. Rice
Keyword(s):  
Animal Model ◽  
Hepatitis C ◽  
Small Animal ◽  
Small Animal Model

scholarly journals The cotton rat provides a useful small-animal model for the study of influenza virus pathogenesis

2005 ◽  
Vol 86 (10) ◽  
pp. 2823-2830 ◽  
Author(s):  
Martin G. Ottolini ◽  
Jorge C. G. Blanco ◽  
Maryna C. Eichelberger ◽  
David D. Porter ◽  
Lioubov Pletneva ◽  
...  
Keyword(s):  
Animal Model ◽  
Influenza Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Cell Damage ◽  
Interleukin 1 ◽  
Small Animal ◽  
Mrna Levels ◽  
Small Animal Model ◽  
Cotton Rats

Influenza A virus continues to cause annual epidemics. The emergence of avian viruses in the human population poses a pandemic threat, and has highlighted the need for more effective influenza vaccines and antivirals. Development of such therapeutics would be enhanced by the use of a small-animal model that is permissive for replication of human influenza virus, and for which reagents are available to dissect the host response. A model is presented of nasal and pulmonary infection in adult inbred cotton rats (Sigmodon hispidus) that does not require viral ‘adaptation’. It was previously demonstrated that animals infected intranasally with 107 TCID50 of a recent H3N2 influenza, A/Wuhan/359/95, have increased breathing rates. In this report it is shown that this is accompanied by weight loss and decreased temperature. Virus replication peaked within 24 h in the lung, with peak titres proportional to the infecting dose, clearing by day 3. Replication was more permissive in nasal tissues, and persisted for 6 days. Pulmonary pathology included early bronchiolar epithelial cell damage, followed by extensive alveolar and interstitial pneumonia, which persisted for nearly 3 weeks. Interleukin 1 alpha (IL1α), alpha interferon (IFN-α), IL6, tumour necrosis factor alpha (TNF-α), GROα and MIP-1β mRNA were elevated soon after infection, and expression coincided with virus replication. A biphasic response was observed for RANTES, IFN-γ, IL4, IL10 and IL12-p40, with increased mRNA levels early during virus replication followed by a later increase that coincided with pulmonary inflammation. These results indicate that cotton rats will be useful for further studies of influenza pathogenesis and immunity.

scholarly journals Viral Persistence and Chronicity in Hepatitis C Virus Infection: Role of T-Cell Apoptosis, Senescence and Exhaustion

Cells ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. 165 ◽  
Author(s):  
Muttiah Barathan ◽  
Rosmawati Mohamed ◽  
Yean Yong ◽  
Meganathan Kannan ◽  
Jamuna Vadivelu ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Responses ◽  
Small Animal ◽  
Viral Escape ◽  
Hepatitis C Virus Infection ◽  
Small Animal Model ◽  
T Cell Apoptosis ◽  
Early Phases

Hepatitis C virus (HCV) represents a challenging global health threat to ~200 million infected individuals. Clinical data suggest that only ~10–15% of acutely HCV-infected individuals will achieve spontaneous viral clearance despite exuberant virus-specific immune responses, which is largely attributed to difficulties in recognizing the pathognomonic symptoms during the initial stages of exposure to the virus. Given the paucity of a suitable small animal model, it is also equally challenging to study the early phases of viral establishment. Further, the host factors contributing to HCV chronicity in a vast majority of acutely HCV-infected individuals largely remain unexplored. The last few years have witnessed a surge in studies showing that HCV adopts myriad mechanisms to disconcert virus-specific immune responses in the host to establish persistence, which includes, but is not limited to viral escape mutations, viral growth at privileged sites, and antagonism. Here we discuss a few hitherto poorly explained mechanisms employed by HCV that are believed to lead to chronicity in infected individuals. A better understanding of these mechanisms would aid the design of improved therapeutic targets against viral establishment in susceptible individuals.

Small Animal Model Systems for Studying Hepatitis B Virus Replication and Pathogenesis

2006 ◽  
Vol 26 (2) ◽  
pp. 181-191 ◽  
Author(s):  
Maura Dandri ◽  
Marc Lutgehetmann ◽  
Tassilo Volz ◽  
Jörg Petersen
Keyword(s):  
Animal Model ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Virus Replication ◽  
Small Animal ◽  
Model Systems ◽  
Small Animal Model ◽  
B Virus

Mechanistic dynamics of Hepatitis C virus replication in single liver cells

2013 ◽  
Vol 51 (01) ◽  
Author(s):  
MM Knodel ◽  
P Targett-Adams ◽  
A Grillo ◽  
S Reiter ◽  
E Herrmann ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Replication ◽  
Liver Cells

Role of autophagy in hepatitis C virus replication

2019 ◽  
Author(s):  
WI Twu ◽  
K Tabata ◽  
D Paul ◽  
R Bartenschlager
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Replication
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