Comparative susceptibility of eastern cottontails and New Zealand white rabbits to classical rabbit haemorrhagic disease virus (RHDV) and RHDV2

Authors

Fawzi Mohamed, USDA ARS Plum Island Animal Disease CenterFollow
Thomas Gidlewski, USDA Animal and Plant Health Inspection Service (APHIS)
Mary L. Berninger, USDA ARS Plum Island Animal Disease Center
Heather M. Petrowski, USDA ARS Plum Island Animal Disease Center
Alexa J. Bracht, USDA ARS Plum Island Animal Disease Center
Carla Bravo de Rueda, USDA ARS Plum Island Animal Disease Center
Roger W. Barrette, USDA ARS Plum Island Animal Disease Center
Meredith Grady, USDA Animal and Plant Health Inspection Service (APHIS)
Emily S. O'Hearn, USDA ARS Plum Island Animal Disease Center
Charles E. Lewis, USDA ARS Plum Island Animal Disease Center
Karen E. Moran, USDA ARS Plum Island Animal Disease Center
Tracy L. Sturgill, USDA Animal and Plant Health Inspection Service (APHIS)
Lorenzo Capucci, Istituto Zooprofilattico Sperimentale della Lombardia e dell'Emilia Romagna Bruno Ubertini
J. Jeffrey Root, USDA APHIS National Wildlife Research CenterFollow

Document Type

Article

Date of this Version

7-1-2022

Citation

Transbound Emerg Dis. 2022;69:e968–e978.

DOI: 10.1111/tbed.14381

Comments

U.S. government work

Abstract

Rabbit haemorrhagic disease virus (RHDV) is associated with high morbidity and mortality in the European rabbit (Oryctolagus cuniculus). In 2010, a genetically distinct RHDV named RHDV2 emerged in Europe and spread to many other regions, including North America in 2016. Prior to this study it was unknown if eastern cottontails (ECT(s); Sylvilagus floridanus), one of the most common wild lagomorphs in the United States, were susceptible to RHDV2. In this study, 10 wild-caught ECTs and 10 New Zealand white rabbits (NZWR(s); O. cuniculus) were each inoculated orally with either RHDV (RHDVa/GI.1a; n = 5 per species) or RHDV2 (a recombinant GI.1bP-GI.2; n = 5 per species) and monitored for the development of disease. Three of the five ECTs that were infected with RHDV2 developed disease consistent with RHD and died at 4 and 6 days post-inoculation (DPI). The RHDV major capsid protein/antigen (VP60) was detected in the livers of three ECTs infected with RHDV2, but none was detected in the ECTs infected with RHDV. Additionally, RHD viral RNA was detected in the liver, spleen, intestine and blood of ECTs infected with RHDV2, but not in the ECTs infected with RHDV. RHD viral RNA was detected in urine, oral swabs and rectal swabs in at least two of five ECTs infected with RHDV2. One ECT inoculated with RHDV2 seroconverted and developed a high antibody titre by the end of the experimental period (21 DPI). ECTs inoculated with the classic RHDV did not seroconvert. In comparison, NZWRs inoculated with RHDV2 exhibited high mortality (five of five) at 2 DPI and four of five NZWRs inoculated with RHDV either died or were euthanized at 2 DPI indicating both of these viruses were highly pathogenic to this species. This experiment indicates that ECTs are susceptible to RHDV2 and can shed viral RNA, thereby suggesting this species could be involved in the epidemiology of this virus.