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Bibert, Stéphanie; Piret, Jocelyne; Quinodoz, Mathieu; Collinet, Emilie; Zoete, Vincent; Michielin, Olivier; Menasria, Rafik; Meylan, Pascal; Bihl, Titus; Erard, Véronique; Fellmann, Florence; Rivolta, Carlo; Boivin, Guy; Bochud, Pierre-Yves
PLoS pathogens, 12/2019, Letnik: 15, Številka: 12Journal Article
We report here two cases of Herpes simplex virus encephalitis (HSE) in adult patients with very rare, previously uncharacterized, non synonymous heterozygous G634R and R203W substitution in mannan-binding lectin serine protease 2 (MASP2), a gene encoding a key protease of the lectin pathway of the complement system. None of the 2 patients had variants in genes involved in the TLR3-interferon signaling pathway. Both MASP2 variants induced functional defects in vitro, including a reduced (R203W) or abolished (G634R) protein secretion, a lost capability to cleave MASP-2 precursor into its active form (G634R) and an in vivo reduced antiviral activity (G634R). In a murine model of HSE, animals deficient in mannose binding lectins (MBL, the main pattern recognition molecule associated with MASP-2) had a decreased survival rate and an increased brain burden of HSV-1 compared to WT C57BL/6J mice. Altogether, these data suggest that MASP-2 deficiency can increase susceptibility to adult HSE.
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