Human TANK-binding kinase 1 is required for early autophagy induction upon herpes simplex virus 1 infection

Mutations disrupting the Toll-like receptor 3 (TLR3) –dependent–interferon pathway can underlie herpes simplex encephalitis (HSE) of childhood caused by herpes simplex virus 1 (HSV1) infection. These otherwise healthy patients with HSE carry germline mutations in the TLR3-interferon circuit, including TIR domain–containing adapter–inducing IFN -β (TRIF) and TANK-binding kinase 1 (TBK1).1,2 Their dermal fibroblasts show impaired interferon production after HSV1 infection and polyinosinic-polycytidylic acid (poly[I:C]) stimulation. (Source: Journal of Allergy and Clinical Immunology)

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