Oral Presentation 12th Australasian Virology Society Meeting 2024

A commercial Japanese encephalitis pig vaccine protects against the newly emerged Genotype IV virus         (#19)

Caitlin A O'Brien 1 , Willy W Suen 1 , Leonard Izzard 1 , Kayla Davis 1 , Grace Taylor 1 , Antonio Di Rubbo 1 , Elise Browne 1 , Stacey E Lynch 1 , David Williams 1
  1. CSIRO - Australian Centre for Disease Preparedness, East Geelong, VIC, Australia

Japanese encephalitis virus (JEV) Genotype IV (GIV) emerged in Australia in 2021-22, resulting in a widespread outbreak across southeastern states and significant economic impacts to the Australian pig industry. Differences in levels of cross-genotype protection (GI–III) have been reported in experimental animal models and field studies in pigs, the major amplifying host and target of vaccine programs in some endemic countries. However, there is limited understanding of the antigenicity of the more divergent GIV virus in pigs, and whether existing commercial GIII-based vaccines are fit for purpose. We established an experimental pig infection model using a 2022 isolate of JEV (NSW/22). Groups of 7–8 pigs received two doses of vaccine or saline (sham) four weeks apart and, at 14 weeks-old, were infected with JEVNSW/22 by intradermal injection. Baseline infection was determined by assessing viraemia, routes of virus shedding, antibody response, tissue tropism and clinical symptoms in sham-vaccinated pigs. Vaccine challenge studies were performed using two vaccination protocols for a commercially available JEV GIII vaccine (Nisseiken): live attenuated/inactivated (JEL/JEK) and inactivated/inactivated (JEK/JEK). Sham-vaccinated pigs infected with JEV GIV were subclinical. Viraemia was detected from day 2 post-infection (dpi) and typically lasted 2 – 5 days, with oral shedding detected from 4dpi. Virus was detected in post-mortem tissues of 8/8 pigs at 21dpi. Following challenge of JEL/JEK vaccinated pigs, viraemia and shedding was not detected in 8/8 pigs and virus was detected in only one pig in post-mortem tissues. Two doses of the inactivated vaccine (JEK/JEK) provided 100% (7/7) protection against both viraemia/shedding and infection. Our pig infection model provides insight into the replication and transmission potential of JEV GIV in the amplifying host. Critically, we have demonstrated that two commercial GIII-based vaccine protocols protect against JEV GIV, providing the basis for potential vaccine options for the Australian pig industry. 

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