Model simulations have shown that the presence of dense colloid particles can either enhance or hinder the horizontal transport of viruses, but also can increase the vertical migration of viruses.
By this means, virus infects the leptomeninges of the brain and subsequent immunopathologic injury dependent on the migration of virus-specific cytotoxic CD8+ T cells into the CNS after their activation and proliferation in the periphery.
This was also expected, assuming that this response reflects the migration of virus-specific lymphocytes to the infected tissue.
Indeed, despite dispensable for SFV fusion which occurs in Rab5-positive endosomes, enrichment with Rab7 and subsequent migration of the virus contained in these Rab7-enriched domains along microtubules was reported for SFV [52].
Again, the DENV-3 phylogeny is compatible with the migration of this virus northward through India to Bhutan.
Despite the lack of understanding of the viral infection processes involved in the migration of the virus from primary infection sites, such as the mucosa in the respiratory or intestinal tracts, to the CNS via the circulation and peripheral nerves, previous studies have described potential pathogenic mechanisms of EV71.
In this study, we track the migration of the H9N2 virus over different regions in mainland China and the Hong Kong SAR using a Bayesian phylogeography approach [ 20].
To examine the changes in genetic diversity during the migration of the H9N2 virus in China, we inferred its demographic history through a Bayesian skyline plots (BSP) coalescent model.
We therefore investigated the effect of virus migration on the estimates of R e. First, we identified lineages that conformed to the assumption of a closed epidemic (i.e., lineages resulting from a single introduction into Australia and New Zealand) and with a sufficiently large local transmission for analysis (i.e., Victoria lineage viruses in 2005, 2006 and 2008).
Estimation of migration of influenza B viruses into and out of Australia and New Zealand.
