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  March, 5 2001 10:01
your information resource in human molecular genetics
As we all know, unless you were prudent and got vaccinated earlier in the season, there’s not much you can do about the flu once you’re infected, apart from taking aspirin, vitamins and hot tea and lying in bed for a couple of days, waiting for your immune system to win the battle against the virus.

Stephan Ludwig and his colleagues at Wuerzburg University in Germany now report on pages 301-305 of the March issue of Nature Cell Biology (Vol. 3, No. 3) how inhibitors of the MAP kinases could be used to prevent viral spreading.

Once it infects a cell, the influenza A virus uses the host cell machinery to proliferate: its genetic material is replicated and translated into viral proteins by the cellular machinery. Viral RNA and viral proteins are then assembled into viral particles, and eventually released from the host cell into the extracellular space, where the newly produced viral particles can infect other cells, starting another cycle of viral replication.

Ludwig and colleagues found that inhibition of the Raf kinase results in inhibition of viral propagation. Why is Raf activity required for viral spreading? When Raf activity is blocked, production of viral material by the host cell is unimpaired, but it is retained in the nucleus and thus cannot propagate to other cells.

But the Raf/MEK/ERK kinases have many other cellular targets, regulating a number of different cellular events such as cell proliferation, cellular differentiation and cell death. So, before the use of these inhibitors as anti-flu drugs can be envisaged, methods need to be developed to target the drugs specifically to virally infected cells if dramatic side effects are to be avoided.

CONTACT: Stephan Ludwig
tel +49 931 201 3851
fax +49 931 201 3835
e-mail: s.ludwig@mail.uni-wuerzburg.de

(C) Nature Cell Biology press release.

Message posted by: Trevor M. D'Souza

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