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AKT capture by feline leukemia virus

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Abstract

Oncogene-containing retroviruses are generated by recombination events between viral and cellular sequences, a phenomenon called “oncogene capture”. The captured cellular genes, referred to as “v-onc” genes, then acquire new oncogenic properties. We report a novel feline leukemia virus (FeLV), designated “FeLV–AKT”, that has captured feline c-AKT1 in feline lymphoma. FeLV–AKT contains a gag–AKT fusion gene that encodes the myristoylated Gag matrix protein and the kinase domain of feline c-AKT1, but not its pleckstrin homology domain. Therefore, it differs structurally from the v-Akt gene of murine retrovirus AKT8. AKT may be involved in the mechanisms underlying malignant diseases in cats.

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Fig. 1
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Abbreviations

FeLV:

Feline leukemia virus

FeLV–AKT :

FeLV containing c-AKT1

FeLV v-AKT :

FeLV viral AKT

gag–AKT :

gag and viral AKT fusion gene

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Acknowledgments

This study was supported by Japan Society for the Promotion of Science KAKENHI.

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Correspondence to Kazuo Nishigaki.

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Funding

This study was funded by Japan Society for the Promotion of Science KAKENHI (Grant Number 15H04602).

Conflict of interest

All authors declare that they have no conflict of interest.

Ethical approval

Animal studies were conducted following the guidelines for the Care and Use of Laboratory Animals of the Ministry of Education, Culture, Sports, Science and Technology, Japan. All experiments were approved by the Genetic Modification Safety Committee of Yamaguchi University.

No studies with human participants were performed.

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Kawamura, M., Umehara, D., Odahara, Y. et al. AKT capture by feline leukemia virus. Arch Virol 162, 1031–1036 (2017). https://doi.org/10.1007/s00705-016-3192-1

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