Deletion of an African Swine Fever Virus ATP-Dependent RNA Helicase QP509L from the Highly Virulent Georgia 2010 Strain Does Not Affect Replication or Virulence

Elizabeth Ramirez-Medina; Elisabeth A Vuono; Sarah Pruitt; Ayushi Rai; Nallely Espinoza; Edward Spinard; Alyssa Valladares; Ediane Silva; Lauro Velazquez-Salinas; Manuel V Borca; Douglas P Gladue

doi:10.3390/v14112548

Deletion of an African Swine Fever Virus ATP-Dependent RNA Helicase QP509L from the Highly Virulent Georgia 2010 Strain Does Not Affect Replication or Virulence

Viruses. 2022 Nov 17;14(11):2548. doi: 10.3390/v14112548.

Authors

Affiliations

¹ Plum Island Animal Disease Center, Agricultural Research Service, United States Department of Agriculture, Greenport, USDA, Greenport, NY 11944, USA.
² Department of Pathobiology and Population Medicine, Mississippi State University, Starkville, MS 39762, USA.
³ Oak Ridge Institute for Science and Education (ORISE), Oak Ridge, TN 37830, USA.
⁴ Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, USA.

Abstract

African swine fever virus (ASFV) produces a lethal disease (ASF) in domestic pigs, which is currently causing a pandemic deteriorating pig production across Eurasia. ASFV is a large and structurally complex virus with a large genome harboring more than 150 genes. ASFV gene QP509L has been shown to encode for an ATP-dependent RNA helicase, which appears to be important for efficient virus replication. Here, we report the development of a recombinant virus, ASFV-G-∆QP509L, having deleted the QP509L gene in the highly virulent field isolate ASFV Georgia 2010 (ASFV-G). It is shown that ASFV-G-∆QP509L replicates in primary swine macrophage cultures as efficiently as the parental virus ASFV-G. In addition, the experimental inoculation of pigs with 10² HAD₅₀ by the intramuscular route produced a slightly protracted but lethal clinical disease when compared to that of animals inoculated with virulent parental ASFV-G. Viremia titers in animals infected with ASFV-G-∆QP509L also had slightly protracted kinetics of presentation. Therefore, ASFV gene QP509L is not critical for the processes of virus replication in swine macrophages, nor is it clearly involved in virus replication and virulence in domestic pigs.

Keywords: ASF; ASFV; African swine fever; African swine fever virus; QP509L; virus virulence.

Publication types

Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

Adenosine Triphosphate
African Swine Fever Virus* / genetics
Animals
DNA Helicases
Georgia
RNA
RNA Helicases
Sus scrofa
Swine
Virulence

Substances

RNA
DNA Helicases
RNA Helicases
Adenosine Triphosphate

Grants and funding

This project was partially and by the National Pork Board Project #21-137 and partially funded through an interagency agreement with the Science and Technology Directorate of the U.S. Department of Homeland Security under Award Number 70RSAT19KPM000056.