November 2015

Event Date: 
Wednesday, November 25, 2015 - 19:00 - 19:45
Institution: 
University of New South Wales
Title: 

Hepatitis C virus – A new age of antiviral therapy

Abstract: 

A wave of new drugs has changed the landscape of hepatitis C virus (HVC) treatment in the last 4-5 years. HCV infection is a major cause of liver cirrhosis, end-stage liver disease and hepatocellular carcinoma. Direct-acting antivirals (DAAs) targeting the HCV RNA-dependent RNA polymerase (RdRp) have shown great success for the treatment of HCV infections. However, the efficacy of DAAs designed to target genotype 1 (G1) HCV against non-G1 viruses has not been characterised fully. Here I overview the changes in the treatment of HCV and investigate the effectiveness of non-nucleoside inhibitors (NNIs) against the HCV RdRp from other genotypes.

Event Date: 
Wednesday, November 25, 2015 - 18:00 - 18:15
Institution: 
University of Sydney
Title: 

Use of synthetic cassettes to detect integron activity in the wild

Abstract: 

Integrons are bacterial genetic elements that enable the capture and expression of exogenous genes, known as ‘gene cassettes’ at a single genomic locus, and are thought to contribute to bacterial adaptation. There is evidence that gene cassettes are shared between bacteria, however to date there is no method of identifying this integron activity in situ.  Here I describe a ‘capture’ approach, whereby synthetically designed gene cassettes with customised selection and detection markers are introduced into complex mixtures of bacteria, enabling the selection of recombinants using appropriate selective media.  This approach should provide valuable insight into what types of bacteria and integrons are involved in active exchange of gene cassettes in natural settings, and a better understanding of the role of integrons in bacterial adaptation.

Event Date: 
Wednesday, November 25, 2015 - 18:15 - 18:30
Institution: 
University of Sydney
Title: 

The role of receptor Smad proteins during Vaccinia virus infection

Abstract: 

VACV infection of cells results in morphological changes reminiscent of epithelial-mesenchymal transition (EMT), a process that occurs during embryonic morphogenesis, cancer metastasis, and wound healing. It is known that EMT is induced by signalling pathways such as the TGF-β/Smad signalling pathway, and previous observations in our lab have indicated elements of this pathway as active following VACV infection. We found that deficiencies in the receptor-Smad proteins (Smad2 and Smad3) not only severely attenuated VACV infection but also prevented characteristic morphological changes normally observed following infection.  Ultimately, these results support a role for VACV-mediated Smad signalling in eliciting an EMT-like phenotype to promote virus spread. This evidence suggests a third role for EMT in pathogenesis, in contrast to the current paradigm of EMT-related events, which are largely restricted to developmental biology and cancer metastasis.