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Unravelling the evolution of antiviral sensors and response systems in animals using the phylum Cnidaria

Project description

Evolution of antiviral response in animals

Antiviral immunity in vertebrates relies on the interferon pathway that enables infected cells to alert neighbouring cells against incoming infection and to recruit immune system cells to battle the virus. In invertebrates, which lack interferons, antiviral immunity is believed to be based mostly on RNA interference that cleaves and inactivates viral RNA. The EU-funded project AntiViralEvo will study the original mode of action of these systems in the latest common ancestors to determine how antiviral immunity was triggered in early animals. Researchers will use the sea anemone Nematostella vectensis, a representative model species of Cnidaria, a phylum that diverged approximately 600 million years ago from other animals. Nematostella is a well-studied lab model and application of advanced molecular and gene manipulation tools will help to decipher the cnidarian system for battling RNA viruses and to answer important questions regarding the evolution of antiviral immunity and its ancestral state in animals.

Objective

Viruses are absolute parasites as their replication depends on biochemical systems of their host. Because viral infections reduce the fitness of the host organism, hosts and viruses have been tangled in an evolutionary arms race for survival from the very beginning of life. As the immune system allows organisms to identify and eliminate viral infections, it is of pivotal importance for host fitness. In vertebrates, the antiviral immunity is heavily based on the interferon pathway that enables infected cells to alert neighbouring cells against incoming infection and recruits cells of the immune system to battle the virus. However, in the case of invertebrates, which lack interferons, the antiviral immunity is believed to be based mostly on an RNA interference (RNAi) that cleaves viral RNA. Until now, the recognition mechanism and mode of action of such systems were studied mostly in vertebrates, insects and nematodes. From this limited phyletic sampling, it is impossible to deduce what was the original mode of action of these systems in their last common ancestor and how antiviral immunity was triggered in early animals. To attain novel insights into the early evolution of this crucial system, I propose to study it in an outgroup: the sea anemone Nematostella vectensis, a representative model species of Cnidaria, a phylum that diverged approximately 600 million years ago from the rest of animals. Beyond its key phyletic position, Nematostella is a tractable lab model with available advanced molecular and gene manipulation tools making it an excellent comparative model. I will harness these tools to decipher the cnidarian system for battling RNA viruses and answer the outstanding questions regarding the evolution of antiviral immunity and its ancestral state in animals. My preliminary results put in question the textbook dichotomy between the antiviral immune systems of vertebrates and invertebrates as I find active components of both systems in Nematostella.

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Programme(s)

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Topic(s)

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Funding Scheme

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ERC-COG - Consolidator Grant

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Call for proposal

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(opens in new window) ERC-2019-COG

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Host institution

THE HEBREW UNIVERSITY OF JERUSALEM
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 998 750,00
Address
EDMOND J SAFRA CAMPUS GIVAT RAM
91904 JERUSALEM
Israel

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Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 1 998 750,00

Beneficiaries (1)

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