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RNA virus packaging specificity explained?

In 1969 David Baltimore proposed that poliovirus RNA replication is coupled with packaging, in that only those genomes actively replicating will be selectively encapsidated. From an evolutionary standpoint, it is an ingenious requirement to ensure that only virus genomes capable of replication are to be passed on to the next cell/host. Furthermore, a virus needs to ensure that all or at the least, the majority of the nucleic acids it packages are derived from its own genome, as opposed to the hosts. Understandably this mechanism is widespread in the virus world where it has been observed in multiple taxa of viruses infecting humans, insects, and plants.
The precise mechanism however, has since been elusive. One mechanism proposed in 1999 by Nugent et. al. hypothesized that a physical interaction occurs between capsid proteins and the RNA replication complex (attached image)(http://jvi.asm.org/content/73/1/427.full). Using Flock house virus (FHV) as a model, the authors in the selected paper, found direct evidence in support of such a hypothesis.
Evidence for the interaction between the viral replicase (Protein A) and the capsid protein was found using bimolecular fluorescence complimentation (http://en.wikipedia.org/wiki/Bimolecular_fluorescence_complementation). Importantly, they showed that this interaction occurs on the outer membranes of the mitochondria, the site of FHV replication.
The authors also found that since Protein A has a mitochondrial trafficking signal, and the capsid protein does not, the interaction was sufficient to support the trafficking of the capsid to the mitochondria. Lastly, they found a trafficking signal specific to the endoplasmic reticulum within the capsid protein as well, also important for packaging.
Thus, this exciting paper has brought forth convincing evidence partially explaining a widespread mechanism in RNA virus packaging specificity.

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