You wait ages for a new ome to come along, and then you hear two in the same talk.
You wait ages for a new ome to come along, and then you hear two in the same talk.
First, there’s the ‘virhostome’, which is short for virus-host interactome. This describes all the ways in which the proteins of a virus interact with those of its host. Effectively, viruses hack into the protein networks within the host cell, and take it over.
Natali Gulbahce combined (mashed up?) the virhostome for the Epstein Barr Virus with a gene-disease map to create what she calls the ‘EBV diseasome network’. This gives a map of the interconnections between viruses, proteins, genes and diseases. It’s a way to tie diseases to viruses – something we already have a pretty good idea of in this case, as the network approach basically recovered all the illnesses previously thought linked to EBV – and to get a handle on the mechanisms by which bugs cause bother.
She then took it to the population level, analysing medical records to compare the patterns of co-occurrence of the diseases of EBV – how many people with mononucleosis, for example, also get lymphoma? – with the positions in the network of the molecules behind them. Such diseases tend to be associated with nearby bits of the diseasome network.
Ultimately, Gulbahce told NetSci 08, besides revealing such patterns and aiding diagnosis, mapping these pathways might help us identify their weak spots – the parts of the virhostome or the links between genes and diseases most vulnerable to disruption. And it might help show how genetic variation contributes to different peoples’ differing susceptibility to disease.
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