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 Carissimo, Guillaume A1 Teo, Teck-Hui A1 Chan, Yi-Hao A1 Lee, Cheryl Yi-Pin A1 Lee, Bernett A1 Torres-Ruesta, Anthony A1 Tan, Jeslin JL A1 Chua, Tze-Kwang A1 Fong, Siew-Wai A1 Lum, Fok-Moon A1 Ng, Lisa FP YR 2019 UL http://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.