colorful character. The influenza virus goes to the house in human cells and diverts our protein for its own purposes.
CDC
Humans are the best friend of the influenza virus. We give a home. We travel and introduce it to new people. We also provide the nasty invaders with hundreds of our own proteins to help get into our cells and copy itself, as a new study Nature and two in Cell show. While this may seem bad news for us, researchers hope that a better understanding of how we aid and abet the enemy make the virus easier to stop.
Together the three studies map the complex interactions between viral and host genes, a feat achieved for some other viruses to date. But this is just a first draft, and the results of different laboratories are both illuminating and confusing. "The three studies are fantastic," said Sumit Chanda, a systems biologist at the Burnham Institute for Medical Research in San Diego, California, who led a team that published one of the reports online December 21 in Nature . "but everyone brings weaknesses and strengths to the table."
the three laboratories identified several hundred human genes that the flu turns to his advantage, but in the most cases, the groups each hit on different ones: Only about 30 genes overlap, a result that is "very surprising," said Peter Palese, a virologist at the Mount Sinai School of Medicine in New York, who co-authored the paper with Chanda. the two related studies that have appeared online December 17 in cell were led by Stephen Elledge at Brigham and Women's hospital in Boston and Sagi Nir Hacohen Shapira and the Broad Institute in Cambridge , Massachusetts.
Yet even these divergent findings open the door to attack the influenza virus by targeting host proteins rather than the unwanted visitor himself. Current antiviral drugs against influenza, such as Tamiflu, cripple essential proteins of the virus itself, but the flu often develop resistance to them. A better strategy would be to focus on how human cells offer the flu a comfortable home. "It would be very difficult for the virus to develop resistance against a therapy that targets a cell protein," says Palese.
But the first researchers must identify the most important proteins and sort the differences between the three groups. Elledge and Chanda teams used the same basic technique to identify important human genes. They mixed the viruses with human cells, then off human genes one at a time with what is called RNA interference. This revealed specific contributors to the welfare of the flu. They now share their raw data, hoping to adjust how their different experimental conditions have led to conflicting results.
the third study, conducted by Shapira and Hacohen Broad, used a completely different strategy, analysis of the interactions between human and viral proteins, and the levels of different expression genes. This "multi-layer" approach provides more of a big-picture look at the host-pathogen dance the finer-grained results of RNA interference studies.
One of the most intriguing discoveries came out of a choice in the laboratory Elledge hunting for human proteins that interfere with the replication of influenza virus, as opposed those who help him. Elledge, who worked with Abraham Brass Massachusetts General Hospital in Boston, found a whole family of these, called interferon-inducible transmembrane proteins. These IFITMs exist in many other species, and Elledge suggests removing from chicken embryos or animal cells that are used to make vaccines against the flu can greatly boost vaccine production by allowing the virus to be more copies of itself. Comparing the levels of these IFITMs in different people may also explain why some people are more susceptible to influenza virus
Memo flu: .. You are not a friend, and your benefits may be about to expire
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