Pathogenetic Potential Relating to Metabolic Activity in a Mouse Model of Infection with the Chikungunya Virus East/Central/South African Genotype

• Published in: Viruses Vol. 12; no. 2; p. 169
• Main Authors: Ngwe Tun, Mya Myat, Muthugala, Rohitha, Kyaw Kyaw, Aung, Shimada, Satoshi, Morita, Kouichi, Hayasaka, Daisuke
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI 03.02.2020; MDPI AG
• Subjects: Africa; Animals; Brain - virology; Central Nervous System - virology; Chikungunya Fever - physiopathology; Chikungunya Fever - virology; Chikungunya virus - genetics; Chikungunya virus - metabolism; Chikungunya virus - pathogenicity; chikv; Disease Models, Animal; ecsa; Genotype; ifn-γ; Mice; mouse model; Phylogeny; Viral Load; viral pathogenesis; Africa; viral pathogenesis; IFN-γ; mouse model; ECSA; CHIKV
• ISSN: 1999-4915; 1999-4915
• DOI: 10.3390/v12020169

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-γ 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.