RT Journal Article SR Electronic T1 Viperin controls chikungunya virus–specific pathogenic T cell IFNγ Th1 stimulation in mice JF Life Science Alliance JO Life Sci. Alliance FD Life Science Alliance LLC SP e201900298 DO 10.26508/lsa.201900298 VO 2 IS 1 A1 Guillaume Carissimo A1 Teck-Hui Teo A1 Yi-Hao Chan A1 Cheryl Yi-Pin Lee A1 Bernett Lee A1 Anthony Torres-Ruesta A1 Jeslin JL Tan A1 Tze-Kwang Chua A1 Siew-Wai Fong A1 Fok-Moon Lum A1 Lisa FP Ng YR 2019 UL https://www.life-science-alliance.org/content/2/1/e201900298.abstract 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.