PT  - JOURNAL ARTICLE
AU  - Guillaume Carissimo
AU  - Teck-Hui Teo
AU  - Yi-Hao Chan
AU  - Cheryl Yi-Pin Lee
AU  - Bernett Lee
AU  - Anthony Torres-Ruesta
AU  - Jeslin JL Tan
AU  - Tze-Kwang Chua
AU  - Siew-Wai Fong
AU  - Fok-Moon Lum
AU  - Lisa FP Ng
TI  - <em>Viperin</em> controls chikungunya virus–specific pathogenic T cell IFNγ Th1 stimulation in mice
AID  - 10.26508/lsa.201900298
DP  - 2019 Feb 01
TA  - Life Science Alliance
PG  - e201900298
VI  - 2
IP  - 1
4099  - https://www.life-science-alliance.org/content/2/1/e201900298.short
4100  - https://www.life-science-alliance.org/content/2/1/e201900298.full
SO  - Life Sci. Alliance2019 Feb 01; 2
AB  - Chikungunya virus (CHIKV) has been a worldwide threat since its reemergence in La Reunion Island in 2004. Expression of the interferon-stimulated protein Viperin correlates with viral load burden in patients, and studies in mice have demonstrated its role to limit disease severity against CHIKV infection. Using Viperin−/− mice, we aimed to understand the contribution of Viperin to the T-cell immune response against CHIKV. CD4 T-cell depletion in Viperin−/− mice showed that increased late acute joint inflammation (5–8 d postinfection) was exclusively mediated by T cells. Specifically, CHIKV-infected Viperin−/− mice showed an increased INFγ Th1 profile of CD4 T cells, enhanced INFγ stimulation by APCs, an increased INFγ secretion profile in the joint microenvironment, and increased numbers of inflammatory monocytes in virus-infected joints compared with WT mice. Bone marrow grafting experiments showed that Viperin expression in both hematopoietic and non-hematopoietic cells is instrumental in reducing disease severity associated with a CD4 T-cell response.