Role of Nora virus VP3 protein in Drosophila melanogaster infection. Sajna Anand Sadanandan^1*, Jens-Ola EkstrÖm¹, Dan Hultmark^1,2. 1) DEPARTMENT OF MOLECULAR BIOLOGY, UMEÅ UNIVERSITY, UMEÅ, SWEDEN; 2) INSTITUE OF BIOMEDICAL TECHNOLOGY, UNIVERSITY OF TAMPERE, TAMPERE, FINLAND.

   Nora virus is a picorna-like virus causing persistent, non-pathological infection in Drosophila melanogaster. Nora virus genome consists of four open reading frames (ORF), where the C-terminus of the ORF1-encoded VP1 protein is an RNAi inhibitor, ORF2 encodes the replicative cassette and ORF4 encodes the major capsid proteins. The function of the ORF3-encoded VP3 protein is under investigation. On gel electrophoresis of viral proteins from purified virus particles, VP3 appears with the VP4 capsid proteins, suggesting that it is involved with the viral capsid. To further study the role of VP3 we constructed mutants 1) where we introduced stop codons such that expression of VP3 is eliminated 2) where we removed 54 nucleotides within the predicted coiled-coil domain of VP3. The effect of these mutations was tested in a wild-type fly stock. The first mutant, wherein VP3 is not produced, affects the transmission of the virus. Viral genome replication could be detected in animals injected with an infective cDNA construct, but not in their offspring. On analyzing for presence of virus particles from injected animals and their feces, we could detect virus particles only in the whole flies. These results suggest that the absence of VP3 makes Nora virus incapable of transmission via the fecal-oral route.