Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro

Oxana V. Denisova; Sandra Sod̈erholm; Salla Virtanen; Carina Von Schantz; Dmitrii Bychkov; Elena Vashchinkina; Jens Desloovere; Janne Tynell; Niina Ikonen; Linda L. Theisen; Tuula A. Nyman; Sampsa Matikainen; Olli Kallioniemi; Ilkka Julkunen; Claude P. Muller; Xavier Saelens; Vladislav V. Verkhusha; Denis E. Kainov

doi:10.1128/AAC.02798-13

Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro

Oxana V. Denisova, Sandra Sod̈erholm, Salla Virtanen, Carina Von Schantz, Dmitrii Bychkov, Elena Vashchinkina, Jens Desloovere, Janne Tynell, Niina Ikonen, Linda L. Theisen, Tuula A. Nyman, Sampsa Matikainen, Olli Kallioniemi, Ilkka Julkunen, Claude P. Muller, Xavier Saelens, Vladislav V. Verkhusha, Denis E. Kainov

Genetics

Research output: Contribution to journal › Article › peer-review

37 Scopus citations

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.

Original language	English (US)
Pages (from-to)	3689-3696
Number of pages	8
Journal	Antimicrobial agents and chemotherapy
Volume	58
Issue number	7
DOIs	https://doi.org/10.1128/AAC.02798-13
State	Published - Jul 2014

ASJC Scopus subject areas

Pharmacology
Pharmacology (medical)
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1128/AAC.02798-13

Cite this

Denisova, O. V., Sod̈erholm, S., Virtanen, S., Von Schantz, C., Bychkov, D., Vashchinkina, E., Desloovere, J., Tynell, J., Ikonen, N., Theisen, L. L., Nyman, T. A., Matikainen, S., Kallioniemi, O., Julkunen, I., Muller, C. P., Saelens, X., Verkhusha, V. V., & Kainov, D. E. (2014). Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro. Antimicrobial agents and chemotherapy, 58(7), 3689-3696. https://doi.org/10.1128/AAC.02798-13

Denisova, OV, Sod̈erholm, S, Virtanen, S, Von Schantz, C, Bychkov, D, Vashchinkina, E, Desloovere, J, Tynell, J, Ikonen, N, Theisen, LL, Nyman, TA, Matikainen, S, Kallioniemi, O, Julkunen, I, Muller, CP, Saelens, X, Verkhusha, VV & Kainov, DE 2014, 'Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro', Antimicrobial agents and chemotherapy, vol. 58, no. 7, pp. 3689-3696. https://doi.org/10.1128/AAC.02798-13

@article{47172abeb8354ddbab86a67e477d99b5,

title = "Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro",

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.",

author = "Denisova, {Oxana V.} and Sandra So{\"d}erholm and Salla Virtanen and {Von Schantz}, Carina and Dmitrii Bychkov and Elena Vashchinkina and Jens Desloovere and Janne Tynell and Niina Ikonen and Theisen, {Linda L.} and Nyman, {Tuula A.} and Sampsa Matikainen and Olli Kallioniemi and Ilkka Julkunen and Muller, {Claude P.} and Xavier Saelens and Verkhusha, {Vladislav V.} and Kainov, {Denis E.}",

year = "2014",

month = jul,

doi = "10.1128/AAC.02798-13",

language = "English (US)",

volume = "58",

pages = "3689--3696",

journal = "Antimicrobial agents and chemotherapy",

issn = "0066-4804",

publisher = "American Society for Microbiology",

number = "7",

}

TY - JOUR

T1 - Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro

AU - Denisova, Oxana V.

AU - Sod̈erholm, Sandra

AU - Virtanen, Salla

AU - Von Schantz, Carina

AU - Bychkov, Dmitrii

AU - Vashchinkina, Elena

AU - Desloovere, Jens

AU - Tynell, Janne

AU - Ikonen, Niina

AU - Theisen, Linda L.

AU - Nyman, Tuula A.

AU - Matikainen, Sampsa

AU - Kallioniemi, Olli

AU - Julkunen, Ilkka

AU - Muller, Claude P.

AU - Saelens, Xavier

AU - Verkhusha, Vladislav V.

AU - Kainov, Denis E.

PY - 2014/7

Y1 - 2014/7

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84903140700&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84903140700&partnerID=8YFLogxK

U2 - 10.1128/AAC.02798-13

DO - 10.1128/AAC.02798-13

M3 - Article

C2 - 24752266

AN - SCOPUS:84903140700

SN - 0066-4804

VL - 58

SP - 3689

EP - 3696

JO - Antimicrobial agents and chemotherapy

JF - Antimicrobial agents and chemotherapy

IS - 7

ER -

Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this