Herpes simplex virus encephalitis in a patient with complete TLR3 deficiency: TLR3 is otherwise redundant in protective immunity.

doi:10.1084/jem.20101568

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Article

Herpes simplex virus encephalitis in a patient with complete TLR3 deficiency: TLR3 is otherwise redundant in protective immunity.

The Journal of experimental medicine - 26 Sept 2011

Guo Yiqi, Audry Magali, Ciancanelli Michael, Alsina Laia, Azevedo Joana, Herman Melina, Anguiano Esperanza, Sancho-Shimizu Vanessa, Lorenzo Lazaro, Pauwels Elodie, Philippe Paul Bastard, Pérez de Diego Rebeca, Cardon Annabelle, Vogt Guillaume, Picard Capucine, Andrianirina Zafitsara Zo, Rozenberg Flore, Lebon Pierre, Plancoulaine Sabine, Tardieu Marc, Valérie Doireau, Jouanguy Emmanuelle, Chaussabel Damien, Geissmann Frederic, Abel Laurent, Casanova Jean-Laurent, Zhang Shen-Ying

Abstract excerpt

Autosomal dominant TLR3 deficiency has been identified as a genetic etiology of childhood herpes simplex virus 1 (HSV-1) encephalitis (HSE). This defect is partial, as it results in impaired, but not abolished induction of IFN-β and -λ in fibroblasts in response to TLR3 stimulation. The apparently normal resistance of these patients to other infections, viral illnesses in particular, may thus result from residual...

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PMID: 21911422
DOI: 10.1084/jem.20101568
PMCID: PMC3182056

Genes

TLR3

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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