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Abstract
The endemic non-pathogenic Australian rabbit calicivirus RCV-A1 is known to provide some cross protection to lethal infection with the closely related Rabbit Haemorrhagic Disease Virus (RHDV). Despite its obvious negative impacts on viral biocontrol of introduced European rabbits in Australia, little is known about the extent and mechanisms of this cross protection. In this study 46 rabbits from a colony naturally infected with RCV-A1 were exposed to RHDV. Survival rates and survival times did not correlate with titres of serum antibodies specific to RCV-A1 or cross reacting to RHDV, but were instead influenced by the time between infection with the two viruses, demonstrating for the first time that the cross protection to lethal RHDV infection is transient. These findings are an important step towards a better understanding of the complex interactions of co-occurring pathogenic and non-pathogenic lagoviruses.
Highlights
The prototype of the genus Lagovirus within the family Caliciviridae is Rabbit Haemorrhagic Disease Virus (RHDV) [1]
We further investigated if the cross protection is dependent on the titres of antibodies raised against Rabbit Calicivirus Australia 1 (RCV-A1) and cross reacting to RHDV
The aim of this study was to assess if cross protection is dependent on the titres of RCV-A1-induced antibodies cross reacting to RHDV, and if there is a difference depending on the infectious dose of RHDV received
Summary
The prototype of the genus Lagovirus within the family Caliciviridae is Rabbit Haemorrhagic Disease Virus (RHDV) [1]. In 1996, RHDV was officially approved for release as a rabbit biocontrol agent in Australia [10], and was very successful in reducing rabbit numbers initially [13] It did not kill rabbits very effectively in some areas of Australia, and in rabbits from these regions antibodies cross reacting to RHDV were found [14]. This lead to the hypothesis that related endemic caliciviruses were circulating in these rabbits, providing some level of cross protection to lethal RDHV infection [15,16]. Pilot infection studies showed that RCV-A1 causes a non-pathogenic infection of the small intestine and is capable of providing partial cross protection to lethal RHDV infection [19], confirming RCV-A1 is hindering effective RHDV-mediated rabbit biocontrol
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