Disabling poxvirus pathogenesis by inhibition of Abl-family tyrosine kinases

@article{Reeves2005DisablingPP,
  title={Disabling poxvirus pathogenesis by inhibition of Abl-family tyrosine kinases},
  author={Patrick M. Reeves and Bettina Bommarius and Sarah W Lebeis and S Mcnulty and J Christensen and Alyson Swimm and Ann Chahroudi and Rahul Chavan and Mark B. Feinberg and Darren R. Veach and William G. Bornmann and Melanie A. Sherman and Daniel Kalman},
  journal={Nature Medicine},
  year={2005},
  volume={11},
  pages={731-739}
}
The Poxviridae family members vaccinia and variola virus enter mammalian cells, replicate outside the nucleus and produce virions that travel to the cell surface along microtubules, fuse with the plasma membrane and egress from infected cells toward apposing cells on actin-filled membranous protrusions. We show that cell-associated enveloped virions (CEV) use Abl- and Src-family tyrosine kinases for actin motility, and that these kinases act in a redundant fashion, perhaps permitting motility… 
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Vaccinia virus p37 interacts with host proteins associated with LE-derived transport vesicle biogenesis
TLDR
The results suggest that p37 localizes to the LE and interacts with proteins associated with LE-derived transport vesicle biogenesis to facilitate assembly of extracellular forms of virus.
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TLDR
It is found that septins are recruited to vaccinia virus immediately after its fusion with the plasma membrane during viral egress, and this antiviral effect is overcome by dynamin together with formin-mediated actin polymerization.
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