Rxivist logo

Rxivist combines preprints from bioRxiv with data from Twitter to help you find the papers being discussed in your field. Currently indexing 73,834 bioRxiv papers from 321,396 authors.

Entry by multiple picornaviruses is dependent on a pathway that includes TNK2, WASL and NCK1

By Hongbing Jiang, Christian Leung, Stephen Tahan, David Wang

Posted 16 Aug 2019
bioRxiv DOI: 10.1101/737635 (published DOI: 10.7554/eLife.50276)

Comprehensive knowledge of the host factors required for picornavirus infection would facilitate antiviral development. Here we demonstrate roles for three human genes, TNK2, WASL, and NCK1, in infection by multiple picornaviruses. CRISPR deletion of TNK2, WASL or NCK1 reduced encephalomyocarditis virus (EMCV), coxsackievirus B3 (CVB3), poliovirus and enterovirus D68 infection, and chemical inhibitors of TNK2 and WASL decreased EMCV infection. Reduced EMCV lethality was observed in mice lacking TNK2. TNK2, WASL and NCK1 were important in early stages of the viral lifecycle, and genetic epistasis analysis demonstrated that the three genes function in a common pathway. Mechanistically, reduced internalization of EMCV was observed in TNK2 deficient cells demonstrating that TNK2 functions in EMCV entry. Domain analysis of WASL demonstrated that its actin nucleation activity was necessary to facilitate viral infection. Together, these data support a model wherein TNK2, WASL, and NCK1 comprise a pathway critical for multiple picornaviruses.

Download data

  • Downloaded 143 times
  • Download rankings, all-time:
    • Site-wide: 63,923 out of 73,834
    • In microbiology: 4,858 out of 6,031
  • Year to date:
    • Site-wide: 35,070 out of 73,834
  • Since beginning of last month:
    • Site-wide: 35,070 out of 73,834

Altmetric data

Downloads over time

Distribution of downloads per paper, site-wide


Sign up for the Rxivist weekly newsletter! (Click here for more details.)