@article{oai:nagasaki-u.repo.nii.ac.jp:00000499,
 author = {Ngwe, Tun  Mya Myat and Muthugala, Rohitha and Kyaw, Kyaw  Aung and Shimada, Satoshi and Morita, Kouichi and Hayasaka, Daisuke},
 issue = {2},
 journal = {Viruses},
 month = {Feb},
 note = {Epidemics of the Chikungunya virus (CHIKV) from 2004 onwards were caused by the East/Central/South African (ECSA) genotype. However, the pathogenesis of the genotype infection has not been fully explained. In this study, we examined the pathogenic potential of CHIKV ECSA genotype M-30 (M-30) by comparing it with that of African genotype S-27 (S-27) in mice. Following low titer infections in type-I IFN receptor KO (A129) mice, we found that the M-30 infection caused high and acute fatality compared with the S-27 infection. M-30-infected A129 mice showed higher viral loads in their central nervous systems and peripheral organs, and increased levels of IFN- responses in their brains. Interestingly, M-30-infected mice did not show the hypophagia and reductions in weight which were observed in S-27-infected mice. Our observations provide a novel explanation of the pathogenic mechanisms attributed to virus proliferation, anti-type-II IFN response and metabolic activity in the CHIKV ECSA virus in mice., Viruses, 12(2), art.no.169; 2020},
 title = {Pathogenetic Potential Relating to Metabolic Activity in a Mouse Model of Infection with the Chikungunya Virus East/Central/South African Genotype},
 volume = {12},
 year = {2020}
}