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The viral landscape of the honey bee (Apismellifera) has changed as a consequence of the global spread of the parasitic mite Varroa destructor and accompanying virulent strains of the iflavirus deformed wing virus (DWV), which the mite vectors. The presence of DWV in honey bee populations is known to influence the occurrence of other viruses, suggesting that the current known virome of A. mellifera may be undercharacterized. Here we tested this hypothesis by examining the honey bee virome in Australia, which is uniquely free of parasitic mites or DWV. Using a high-throughput sequencing (HTS) approach, we examined the RNA virome from nine pools of A. mellifera across Australia. In addition to previously reported honey bee viruses, several other insect viruses were detected, including strains related to aphid lethal paralysis virus (ALPV) and Rhopalosiphum padi virus (RhPV), which have recently been identified as infecting honey bees in the USA, as well as several other viruses recently found in Drosophila spp. A further 42 putative novel insect virus genomes spanning the order Picornavirales were assembled, which significantly increases the known viral diversity in A. mellifera. Among these novel genomes, we identified several that were similar (but different) to key A. mellifera viruses, such as DWV, that warrant further investigation. We propose that A. mellifera may be preferentially infected with viruses of the order Picornavirales and that a diverse population of these viruses may be representative of a Varroa-free landscape.

West Nile virus (WNV; family Flaviviridae; genus Flavivirus) group members are an important cause of viral meningoencephalitis in some areas of the world. They exhibit marked variation in pathogenicity, with some viral lineages (such as those from North America) causing high prevalence of severe neurological disease, whilst others (such as Australian Kunjin virus) rarely cause disease. The aim of this study was to characterize WNV disease in a mouse model and to elucidate the pathogenetic features that distinguish disease variation. Tenfold dilutions of five WNV strains (New York 1999, MRM16 and three horse isolates of WNV-Kunjin: Boort and two isolates from the 2011 Australian outbreak) were inoculated into mice by the intraperitoneal route. All isolates induced meningoencephalitis in different proportions of infected mice. WNVNY99 was the most pathogenic, the three horse isolates were of intermediate pathogenicity and WNVKUNV-MRM16 was the least, causing mostly asymptomatic disease with seroconversion. Infectivity, but not pathogenicity, was related to challenge dose. Using cluster analysis of the recorded clinical signs, histopathological lesions and antigen distribution scores, the cases could be classified into groups corresponding to disease severity. Metrics that were important in determining pathotype included neurological signs (paralysis and seizures), meningoencephalitis, brain antigen scores and replication in extra-neural tissues. Whereas all mice infected with WNVNY99 had extra-neural antigen, those infected with the WNV-Kunjin viruses only occasionally had antigen outside the nervous system. We conclude that the mouse model could be a useful tool for the assessment of pathotype for WNVs., (© 2014 CSIRO.)