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Thesis summary: 

The family Picornaviridae encompasses several notorious human and animal pathogens including poliovirus (genus Enterovirus), hepatitis A virus (genus Hepatovirus) and foot-and-mouth disease virus (genus Aphthovirus). In 1898, foot-and-mouth disease virus was the first ‘infectious agent smaller than a bacteria that could transmit disease amongst animals’ that was discovered. Shortly after, in 1908, poliovirus was the first identified virus that transmits disease in humans. Although these pathogens were called viruses, the Latin term for poison, it was largely unknown what these pathogens were or how they transmitted disease. Since their discovery, these two viruses have been studied extensively and had a vital role in the development of the field of molecular virology. Understanding how these viruses translate and replicate their genome, as well as how they manipulate cellular processes, has also contributed to our current understanding of the molecular processes of the cell.

Viruses are acellular parasites that are dependent on their hosts metabolism for their replication. Replication of picornaviruses, like for all other viruses, can be recognized by their hosts and this triggers the activation of antiviral responses. Viruses must counteract these antiviral responses in order to spread to neighboring tissues and successfully establish infection. In this thesis, we study how selected picornaviruses evade innate antiviral responses. We uncovered molecular mechanisms utilized by enteroviruses, foot-and-mouth disease virus and the human aichivirus to evade the induction of type I interferon and/or the cellular stress response.