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In the present study, we report that MITA undergoes DDOST-mediated N-glycosylation in the endoplasmic reticulum (ER) upon DNA viral infection. Selective mutation of DDOST-dependent N-glycosylated residues abolished MITA oligomerization and thereby its immune functions. Moreover, increasing the expression of Ddost in the mouse brain effectively strengthens the local immune response to herpes simplex virus-1 (HSV-1) and prolongs the survival time of mice with HSV encephalitis (HSE). Our findings reveal the dependence of N-glycosylation on MITA activation and provide a new perspective on the pathogenesis of HSE.<\/jats:p>","DOI":"10.1371\/journal.ppat.1010989","type":"journal-article","created":{"date-parts":[[2022,11,30]],"date-time":"2022-11-30T13:33:08Z","timestamp":1669815188000},"page":"e1010989","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":13,"title":["MITA oligomerization upon viral infection is dependent on its N-glycosylation mediated by 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