Herpes simplex encephalitis in children with autosomal recessive and dominant TRIF deficiency.

@article{SanchoShimizu2011HerpesSE,
  title={Herpes simplex encephalitis in children with autosomal recessive and dominant TRIF deficiency.},
  author={Vanessa Sancho-Shimizu and Rebeca P{\'e}rez de Diego and Lazaro Lorenzo and Rabih Halwani and Abdullah A Alangari and Elisabeth Israelsson and Sylvie Fabrega and Annabelle Cardon and J{\'e}r{\^o}me Maluenda and Megumi Tatematsu and Farhad Mahvelati and Melina Herman and Michael J Ciancanelli and Yiqi Guo and Zobaida Alsum and Nouf Alkhamis and AbdulKarim S. Al-Makadma and Ata Ghadiri and Soraya Boucherit and Sabine Plancoulaine and Capucine Picard and Flore Rozenberg and Marc Tardieu and Pierre Lebon and Emmanuelle Jouanguy and Nima Attaran Rezaei and Tsukasa Seya and Misako Matsumoto and Damien Chaussabel and Anne Puel and S Zhang and Laurent Abel and Saleh Zaid Al-Muhsen and J. Hugo P{\'e}rez Casanova},
  journal={The Journal of clinical investigation},
  year={2011},
  volume={121 12},
  pages={4889-902}
}
Herpes simplex encephalitis (HSE) is the most common sporadic viral encephalitis of childhood. Autosomal recessive (AR) UNC-93B and TLR3 deficiencies and autosomal dominant (AD) TLR3 and TRAF3 deficiencies underlie HSE in some children. We report here unrelated HSE children with AR or AD TRIF deficiency. The AR form of the disease was found to be due to a homozygous nonsense mutation that resulted in a complete absence of the TRIF protein. Both the TLR3- and the TRIF-dependent TLR4 signaling… CONTINUE READING
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