| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-102 |
Sentence |
denotes |
Mutations in the TLR3 signaling pathway and beyond in adult patients with herpes simplex encephalitis. |
| TextSentencer_T2 |
103-259 |
Sentence |
denotes |
Herpes simplex encephalitis (HSE) in children has previously been linked to defects in type I interferon production downstream of Toll-like receptor (TLR)3. |
| TextSentencer_T3 |
260-391 |
Sentence |
denotes |
In the present study, we used whole-exome sequencing to investigate the genetic profile of 16 adult patients with a history of HSE. |
| TextSentencer_T4 |
392-565 |
Sentence |
denotes |
We identified novel mutations in IRF3, TYK2 and MAVS, molecules involved in generating innate antiviral immune responses, which have not previously been associated with HSE. |
| TextSentencer_T5 |
566-713 |
Sentence |
denotes |
Moreover, data revealed mutations in TLR3, TRIF, TBK1 and STAT1 known to be associated with HSE in children but not previously described in adults. |
| TextSentencer_T6 |
714-986 |
Sentence |
denotes |
All discovered mutations were heterozygous missense mutations, the majority of which were associated with significantly decreased antiviral responses to HSV-1 infection and/or the TLR3 agonist poly(I:C) in patient peripheral blood mononuclear cells compared with controls. |
| TextSentencer_T7 |
987-1217 |
Sentence |
denotes |
Altogether, this study demonstrates novel mutations in the TLR3 signaling pathway in molecules previously identified in children, suggesting that impaired innate immunity to HSV-1 may also increase susceptibility to HSE in adults. |
| TextSentencer_T8 |
1218-1429 |
Sentence |
denotes |
Importantly, the identification of mutations in innate signaling molecules not directly involved in TLR3 signaling suggests the existence of innate immunodeficiencies predisposing to HSE beyond the TLR3 pathway. |
| T1 |
0-102 |
Sentence |
denotes |
Mutations in the TLR3 signaling pathway and beyond in adult patients with herpes simplex encephalitis. |
| T2 |
103-259 |
Sentence |
denotes |
Herpes simplex encephalitis (HSE) in children has previously been linked to defects in type I interferon production downstream of Toll-like receptor (TLR)3. |
| T3 |
260-391 |
Sentence |
denotes |
In the present study, we used whole-exome sequencing to investigate the genetic profile of 16 adult patients with a history of HSE. |
| T4 |
392-565 |
Sentence |
denotes |
We identified novel mutations in IRF3, TYK2 and MAVS, molecules involved in generating innate antiviral immune responses, which have not previously been associated with HSE. |
| T5 |
566-713 |
Sentence |
denotes |
Moreover, data revealed mutations in TLR3, TRIF, TBK1 and STAT1 known to be associated with HSE in children but not previously described in adults. |
| T6 |
714-986 |
Sentence |
denotes |
All discovered mutations were heterozygous missense mutations, the majority of which were associated with significantly decreased antiviral responses to HSV-1 infection and/or the TLR3 agonist poly(I:C) in patient peripheral blood mononuclear cells compared with controls. |
| T7 |
987-1217 |
Sentence |
denotes |
Altogether, this study demonstrates novel mutations in the TLR3 signaling pathway in molecules previously identified in children, suggesting that impaired innate immunity to HSV-1 may also increase susceptibility to HSE in adults. |
| T8 |
1218-1429 |
Sentence |
denotes |
Importantly, the identification of mutations in innate signaling molecules not directly involved in TLR3 signaling suggests the existence of innate immunodeficiencies predisposing to HSE beyond the TLR3 pathway. |