Figure 1 (Left) Diagram illustrating a rhabdovirus virion and the nucleocapsid structure (courtesy of P. Le Mercier); (right) negative contrast electron micrograph of virions of an isolate of vesicular stomatitis Indiana virus. The bar represents 100 nm.
(Courtesy of P. Perrin.)
Figure 2 Comparison of genome organization of representative members from all genera of the family Rhabdoviridae. A modular organization into three blocks has been conserved: the 3′ block #1 encodes N/P proteins required in large amounts; the central block #2 encodes the membrane M/G proteins; the 5′ block #3 encodes the polymerase L required in limited amounts. Between blocks, viruses have inserted typical genes adapted to their particular biology, for example the movement protein (3, 4b) in plant rhabdoviruses.
(Courtesy of N. Tordo.)
Figure 3 Panel (1) shows the genome organization of vesicular stomatitis Indiana virus (VSIV) and the process of consecutive transcription of leader RNA and monocistronic mRNAs. Panel (2) illustrates the replication of the negative sense genome via a positive sense antigenome intermediate. The switch from transcription to replication appears to be regulated by the N protein.
(Courtesy of P. Le Mercier.)
Figure 4 Architecture of the vesicular stomatitis virus virion. Montage model of the tip and cryoEM map of the trunk. N is green, M is blue, and the inner (2) and outer (1) leaflets of the membrane are violet and pink. (Inset) illustration of the base region of the VSV virion. The “X” marks the absence of a turn of M helix below the lowest turn of the N helix.
(From Ge, P., Tsao, J., Schein, S., Green, T. J., Luo, M. and Zhou, Z. H. (2010). Cryo-EM model of the bullet-shaped vesicular stomatitis virus. Science, 327, 689–93; with permission.)
Figure 5 Contrasts between the replication cycles of cytorhabdoviruses and nucleorhabdoviruses. Most rhabdoviruses gain entry into host cells during insect vector feeding. Uncoating is believed to take place on ER membranes, followed by release of the nucleocapsid core into the cytoplasm. At this point, the replication cycles of the two genera diverge. In the case of the cytorhabdoviruses, the newly released cores become transcriptionally active and associate with the endoplasmic reticulum to establish viroplasms that function in transcription of viral mRNAs (vmRNAs) and replication of genomic and antigenomic viral RNAs. Following translation of the vmRNAs, viral proteins involved in replication accumulate in the viroplasm. Viral glycoproteins are targeted to cytoplasmic membranes or, possibly, the outer nuclear envelope (ONE). Maturation of cytorhabdoviruses takes place via matrix protein-mediated condensation of cores at sites of G protein accumulation in the endoplasmic reticulum. In the case of the nucleorhabdoviruses, released cores are transported into the nucleus through nuclear pore complexes (NPC). Following transcription and export, vmRNAs are translated and viral proteins are imported into the nucleus, where they participate in replication and formation of large viroplasms. During intermediate stages of infection of plant rhabdoviruses, movement of infectious units from cell to cell occurs. Nucleocapsids most likely are the transported form, and these interact with viral encoded movement proteins that participate in number of activities, including nucleocapsid binding, transport through the NPC to the plasmodesmata, and modifications to the plasmodesmatal size exclusion limits. Morphogenesis occurs near the end of active transcription and replication and involves interactions with the M protein to coil the viral nucleocapsids and form associations with membrane-associated G protein. In the cytorhabdoviruses, electron microscopic observations suggest that budding occurs into proliferated ER associated with the viroplasms. Currently, at least two models can be proposed for morphogenesis of nucleorhabdovirus virions. In recent data outlined in the text, the inner nuclear envelope (INE) proliferates due to redistribution of cytoplasmic membranes and invaginates to form intranuclear spherules, into which viral budding occurs. In the classical model, virus budding occurs through intact INE resulting in an expansion of the outer nuclear envelope. In both models, mature virions accumulate in the perinuclear spaces of infected cells where they may be reacquired during subsequent insect feeding.
(Reproduced from Jackson et al. (2005); with permission from Annual Reviews.)
Figure 6 Phylogenetic tree of viruses in the Rhabdoviridae based on alignment of nucleoprotein gene sequences. The tree was generated by the neighbor-joining method using 1000 bootstrap replicates.