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Interactions of Paramyxoviruses and host cells

English title Interactions of Paramyxoviruses and host cells
Applicant Garcin Dominique
Number 116114
Funding scheme Project funding (Div. I-III)
Research institution Dépt Microbiologie et Médecine Moléculaire Faculté de Médecine Université de Genève
Institution of higher education University of Geneva - GE
Main discipline Cellular Biology, Cytology
Start/End 01.04.2007 - 31.03.2010
Approved amount 335'000.00
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Lay Summary (English)

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Lay summary
Viruses are obligatory intracellular parasites and have been present throughout evolution. Animal cells have thus developed multiple mechanisms to protect themselves from the pathogenic effects of virus infection; and viruses have, of course, developed multiple ways to circumvent the cellular defenses. This war has gone on since cells first appeared, and is still on-going. Unlike animal cells, whose genome is large enough to code for as many virus-defense genes as are needed, small RNA viruses like paramyxoviruses have relatively limited genetic capacities. Small RNA viruses, like measles and mumps virus, in fact, produce only 6 mRNAs, and their gene products must not only amplify the viruses, but counteract the host defense during their replication. Viruses which have failed in this latter task are no longer among us. One way in which viruses have extended their coding capacity is exemplified by the Sendai virus P gene. The Sendai virus P gene has long been an example of how a virus (even one that replicates in the cytoplasm) can pack the maximum amount of coding potential into a single gene, using all 3 open reading frames (ORFs) and various translational tricks (non-AUG codons, leaky scanning, and ribosomal shunt) and transcriptionsl tricks (co-transcriptional mRNA editing). The SeV P gene yields a minimum of 7 primary translation products, and except for the P protein (a subunit of the viral RNA polymerase), the other products (C’, C, Y1, Y2, V and W) are strictly non-essential. However, they do play important roles in countering the cellular innate antiviral response, and we are beginning to understand how these various P gene accessory proteins act. C’ and C, e.g., contain a plasma membrane (PM) targeting signal at their N-termini (absent in Y1/Y2), and their concentration at the PM is essential for the activities that are specific to the longer C proteins.
Direct link to Lay Summary Last update: 21.02.2013

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Associated projects

Number Title Start Funding scheme
135467 The molecular basis of ligand recognition by RIG-I and viral escape strategies 01.04.2011 Project funding (Div. I-III)
67280 Replication of paramyxoviruses 01.04.2002 Project funding (Div. I-III)

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