Abstract

It is just over 20 years since the landmark discovery was made by Baltimore et al. (1970) that vesicular stomatitis virus (VSV) packages within the mature virion the vital RNA-dependent RNA polymerase that transcribes the negative sense (anti-message sense) genome RNA into messenger RNAs. This unique observation provided the window of opportunity to study the regulation of VSV gene expression in the test tube and made VSV an early paradigm for RNA viral gene expression, a position that it has maintained ever since. In the past two decades, availability of information pertaining to the mechanism of gene expression of VSV has burgeoned, providing a better understanding of the structure and function of not only the VSV genome and its products but also those of negative-strand RNA viruses in general. The complete nucleotide sequence of the genome is now known (Rose and Schubert, 1987) and hence the sequence of the mRNAs and the deduced amino acid sequences of the viral proteins. All virus-coded proteins have been identified and their possible functions in the viral life cycle assigned. Notwithstanding this progress, the precise mechanisms by which the linear, single-strand RNA genome is transcribed into mRNAs and eventually replicated still remain a challenge to molecular virologists. VSV, a rhabdovirus, is thus a prototype model of all nonsegmented negative-strand RNA viruses, such as rabies, measles, mumps, parainfluenza, respiratory syncytial, and Sendai, to mention a few. While rabies is a rhabdovirus, all the other examples belong to the Paramyxoviridae family. The gene order and overall mechanism of gene expression in these two families of viruses are generally expected to be very similar. Available evidence has in fact demonstrated a commonality in their modes of transcription and replication. However, there are specific differences between VSV and the paramyxoviruses (as there are among the individual members of the Paramyxoviridae family) that warrant

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