Lagovirus europaeus GI.2/RHDV2 (Rabbit Haemorrhagic Disease Virus 2)

• Main Author: Neimanis, Aleksija
• Format: Doctoral or Postdoctoral Thesis
• Language: Swedish; English
• Published: 2018
• Subjects: Pathobiology; Lepus timidus; mountain hare
• Online Access: https://pub.epsilon.slu.se/15594/; https://pub.epsilon.slu.se/15594/1/neimanis_a_180827.pdf

Rabbit haemorrhagic disease (RHD) was first detected in 1984 and quickly spread among wild and domestic European rabbits (Oryctolagus cuniculus) throughout the world. RHD and European brown hare syndrome (EBHS), a related disease of hares (Lepus spp.), are caused by pathogenic lagoviruses of the Family Caliciviridae. Infection of susceptible animals results in a necrotizing, often fatal, hepatitis. The causative viruses known as Lagovirus europaeus GI.1/RHDV and L. europaeus GII.1/EBHSV are considered genus specific, causing disease in Oryctolagus cuniculus and some Lepus spp., respectively. Full susceptibility to clinical disease only occurs after approximately eight weeks of age. This understanding of pathogenic lagoviruses changed in 2010 with the emergence of a new virus, L. europaeus GI.2/RHDV2. While this new lagovirus shares features with the previously described, classic lagoviruses, it can cross species barriers and caused mortality in two southern European hare species, Lepus capensis mediterraneus and Lepus corsicanus. It also infects and kills young rabbits. Studies here explored and helped define this new, expanded paradigm of pathogenic lagoviruses. Susceptibility to GI.2/RHDV2 was described in two new host species, the European brown hare (Lepus europaeus) and the mountain hare (Lepus timidus). Mortality events in hares in Sweden, Italy and Spain provided insight into disease ecology. Infections likely spilled over from GI.2/RHDV2 outbreaks in rabbits, and the mountain hare outbreak lasted several months in the absence of rabbits. Disease caused by GI.2/RHDV2 was compared to classic RHD and EBHS in young and adult rabbits, and adult hares, respectively. In adults, pathology and virus tissue distribution were the same irrespective of the causative virus. In contrast to GI.1/RHDV, GI.2/RHDV2 caused similar disease in 5-week old kittens and adults. This thesis helped map GI.2/RHDV2 emergence by investigating its presence in Sweden. The first confirmed case was in May 2013, but initial cases were diagnosed as classic RHD. Widespread outbreaks did not occur until 2016 and phylogenetic analysis supported virus evolution and/or multiple introductions. Findings in this thesis helped prevent disease in domestic rabbits in Sweden and further our understanding of GI.2/RHDV2. GI.2/RHDV2 provides an excellent opportunity to study how viruses overcome species and age barriers.