1887

Abstract

West Nile virus (WNV) is the leading cause of mosquito-borne illness in the USA. There are currently no human vaccines or therapies available for WNV, and vector control is the primary strategy used to control WNV transmission. The WNV vector is also a competent host for the insect-specific virus (ISV) Eilat virus (EILV). ISVs such as EILV can interact with and cause superinfection exclusion (SIE) against human pathogenic viruses in their shared mosquito host, altering vector competence for these pathogenic viruses. The ability to cause SIE and their host restriction make ISVs a potentially safe tool to target mosquito-borne pathogenic viruses. In the present study, we tested whether EILV causes SIE against WNV in mosquito C6/36 cells and mosquitoes. The titres of both WNV strains – WN02-1956 and NY99 – were suppressed by EILV in C6/36 cells as early as 48–72 h post-superinfection at both m.o.i. values tested in our study. The titres of WN02-1956 at both m.o.i. values remained suppressed in C6/36 cells, whereas those of NY99 showed some recovery towards the final timepoint. The mechanism of SIE remains unknown, but EILV was found to interfere with NY99 attachment in C6/36 cells, potentially contributing to the suppression of NY99 titres. However, EILV had no effect on the attachment of WN02-1956 or internalization of either WNV strain under superinfection conditions. In , EILV did not affect the infection rate of either WNV strain at either timepoint. However, in mosquitoes EILV enhanced NY99 infection titres at 3 days post-superinfection, but this effect disappeared at 7 days post-superinfection. In contrast, WN02-1956 infection titres were suppressed by EILV at 7 days post-superinfection. The dissemination and transmission of both WNV strains were not affected by superinfection with EILV at either timepoint. Overall, EILV caused SIE against both WNV strains in C6/36 cells; however, in , SIE caused by EILV was strain specific potentially owing to differences in the rate of depletion of shared resources by the individual WNV strains.

Funding
This study was supported by the:
  • Huck Institutes of the Life Sciences (Award Dorothy Foehr Huck and J. Lloyd Huck endowment)
    • Principle Award Recipient: JasonL Rasgon
  • Pennsylvania Department of Health (Award Tobacco Settlement Funds)
    • Principle Award Recipient: JasonL Rasgon
  • U.S. Department of Agriculture (Award 4769)
    • Principle Award Recipient: JasonL Rasgon
  • National Science Foundation (Award 1645331)
    • Principle Award Recipient: JasonL Rasgon
  • National Institutes of Health (Award R01AI150251)
    • Principle Award Recipient: JasonL Rasgon
  • National Institutes of Health (Award R01A1128201)
    • Principle Award Recipient: JasonL Rasgon
  • This is an open-access article distributed under the terms of the Creative Commons Attribution License. This article was made open access via a Publish and Read agreement between the Microbiology Society and the corresponding author’s institution.
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2024-08-27
2024-09-15
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