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SUMMARY:Comparisons between how influenza A viruses and parainfluenza viru
 ses interact with the interferon system. - Professor Rick Randell\, Biomol
 ecular Sciences\, School of Biology\, University of St. Andrews\, Scotland
DTSTART:20090603T153000Z
DTEND:20090603T163000Z
UID:TALK17877@talks.cam.ac.uk
CONTACT:Suzy Blows
DESCRIPTION:Small RNA viruses have limited genetic information and therefo
 re many of the virally encoded proteins have multiple functions. As part o
 f their genetic repertoire\, most small RNA viruses also have to produce s
 pecific antagonists of the interferon (IFN) system that\, whilst not essen
 tial for virus replication\, are nevertheless absolutely necessary for vir
 us pathogenesis and survival in nature. Many of these viral IFN antagonist
 s are therefore multifunctional proteins with other roles in the replicati
 on cycle of the virus. Furthermore\, the way in which viruses interact wit
 h the IFN system may play an important role in defining the type of diseas
 e they induce and even their epidemiology. This principle will be illustra
 ted using examples from our work on the NS1 protein of influenza virus and
  the V protein of parainfluenza virus type 5 (PIV 5). For example\, the NS
 1 protein intercedes at multiple points within the cells anti-viral defenc
 e responses\, including binding dsRNA\, inhibiting RIG-I and PKR as well a
 s preventing the correct maturation and export of cellular mRNAs from the 
 nucleus to the cytoplasm. In addition to these inhibitory actions on cellu
 lar processes\, NS1 also specifically activates cellular PI3 kinase\, alth
 ough the biological consequences for this remain unclear. With regards the
  V protein of PIV5\, this protein acts as an IFN antagonist by both limiti
 ng the production of IFN and blocking IFN signalling. The V protein at lea
 st partially inhibits IFN production by binding to mda-5\, an intracellula
 r detector of viruses\, and inhibiting its ability to activate the intrace
 llular signalling c yetascade that leads to the production of IFN-β. To b
 lock IFN signalling\, the V protein specifically targets the cellular tran
 scription factor STAT1 (which is essential for IFN signalling) for proteos
 ome-mediated degradation. In addition\, the V protein also activates AKT a
 nd binds to soluble forms of the nucleocapsid protein and thus has importa
 nt roles to play in controlling transcription and replication of the virus
  genome. Thus\, by further understanding the structure/multifunctional nat
 ure of these small IFN antagonists a better understanding of the molecular
  pathogenesis of these viruses will be achieved and improved mechanisms fo
 r their control may be developed through the design of virus vaccines and 
 development of novel anti-viral drugs.
LOCATION:Lecture Theatre 1\, Department of Veterinary Medicine
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