The replication machinery, along with the viral envelope, is responsible for the unique broad cell tropism of Bungowannah virus.
Envelope not sufficient for Bungowannah tropism; leaves open replication machinery contributions in pestiviruses.
Bungowannah virus is the most divergent pestivirus, and both origin and reservoir host have not been identified so far. We therefore performed in vitro tropism studies, which showed that Bungowannah virus differs remarkably from other pestiviruses. Interestingly, cell lines of vervet monkey, mouse, human and even of bat origin were susceptible. This broad in vitro tropism was not observed for a chimeric bovine viral diarrhoea virus (BVDV) expressing all structural proteins of Bungowannah virus. The viral envelope was not sufficient to completely transfer the cell tropism of Bungowannah virus to another pestivirus, and viral RNA replication was either markedly reduced or not detectable in a number of different cell lines for the tested BVDV strain and the chimera. We therefore suggest that the replication machinery together with the viral envelope is responsible for the unique broad cell tropism of Bungowannah virus.
No takes yet. Share an insight, caveat, or question.
Richter et al. (2014) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: