| Literature DB >> 24752266 |
Oxana V Denisova1, Sandra Söderholm2, Salla Virtanen3, Carina Von Schantz1, Dmitrii Bychkov1, Elena Vashchinkina3, Jens Desloovere1, Janne Tynell4, Niina Ikonen4, Linda L Theisen5, Tuula A Nyman6, Sampsa Matikainen7, Olli Kallioniemi1, Ilkka Julkunen4, Claude P Muller5, Xavier Saelens8, Vladislav V Verkhusha9, Denis E Kainov10.
Abstract
The influenza pH1N1 virus caused a global flu pandemic in 2009 and continues manifestation as a seasonal virus. Better understanding of the virus-host cell interaction could result in development of better prevention and treatment options. Here we show that the Akt inhibitor MK2206 blocks influenza pH1N1 virus infection in vitro. In particular, at noncytotoxic concentrations, MK2206 alters Akt signaling and inhibits endocytic uptake of the virus. Interestingly, MK2206 is unable to inhibit H3N2, H7N9, and H5N1 viruses, indicating that pH1N1 evolved specific requirements for efficient infection. Thus, Akt signaling could be exploited further for development of better therapeutics against pH1N1 virus.Entities:
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Year: 2014 PMID： 24752266 PMCID： PMC4068572 DOI： 10.1128/AAC.02798-13
Source DB: PubMed Journal: Antimicrob Agents Chemother ISSN： 0066-4804 Impact factor: 5.191