paper: viruses classified by the folds they contain

[alwen]

This article,

"Study adds to evidence that viruses are alive"
talks about the paper:
http://phys.org/news/2015-09-evidence-viruses-alive.html

Paper: A phylogenomic data-driven exploration of viral origins and evolution, Science Advances, 2015. DOI: 10.1126/sciadv.1500527

"The new study focused on the vast repertoire of protein structures, called "folds," that are encoded in the genomes of all cells and viruses. Folds are the structural building blocks of proteins, giving them their complex, three-dimensional shapes. By comparing fold structures across different branches of the tree of life, researchers can reconstruct the evolutionary histories of the folds and of the organisms whose genomes code for them.

The researchers chose to analyze protein folds because the sequences that encode viral genomes are subject to rapid change; their high mutation rates can obscure deep evolutionary signals, Caetano-Anollés said. Protein folds are better markers of ancient events because their three-dimensional structures can be maintained even as the sequences that code for them begin to change."

[inkycatz]

Appreciate the link, alwen! :)

[Bruno Kestemont]

Very interesting !

It's written: "Ebola virus, which has only seven genes…"

Does it mean than Ebola can only produce seven proteins himself or isn't it so simple? (it's other proteins being constructed by the host).

As they say that the "own" virus proteins are mainly the caps that protect them, can we conclude that if antibodies or medicines only concentrate on these virus-specific proteins, the chances to be damagable to the host would be minimized ?

Did you provide us one of these (seven?) specific proteins to attack?

[v_mulligan]

In general, "just N genes" does not necessarily mean "just N proteins". Humans, for example, have about 25,000 genes, but about 100,000 proteins, because one gene can be responsible for more than one protein through the magic of splicing and other post-transcriptional or post-translational events. (In lay terms, "I have a recipe that calls for this chain of amino acids, but in this cell, I'll remove this block in the middle, and in that cell, I'll remove this other block in the middle, so I end up with two different products in two different cell types".)

In the case of Ebola, the virus has only 7 genes, and about 7 proteins, depending on what you count as a different protein. There are definitely variant proteins made from the same gene, though. The Ebola glycoprotein, for example, (which is the viral protein that we want you to target), gets made in at least two forms: a virus-bound, functional form necessary for viral invasion of host cells, and a free-floating, secreted form whose function is not fully understood, but which is thought to help the virus evade the immune response by providing "decoys" that antibodies will bind to.

Viruses can also incorporate proteins from the host cells that they infect, and there is some evidence that this happens in the case of Ebola and Marburg, though whether this is important for viral function is not known. Viruses definitely require the action of host cell proteins to allow them to reproduce themselves (a seven-gene genome is not sufficient to encode a self-reproducing organisms), but a lot of that happens in the infected host cells, not in the virus itself.

But yes, we definitely want to go after the proteins that are unique to the virus and which don't have close homologues in the human proteome. This is how antibiotics (for bacterial infection) generally work (disrupting pieces of bacterial machinery without close human homologues) and how current anti-virals, like the HIV protease inhibitors (which disrupt HIV enzymes without close human homologues, which are necessary for HIV viral maturation), work.