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Isolation of Brain-infiltrating Leukocytes

Isolation of Brain-infiltrating Leukocytes

Published on: June 13, 2011

Herpes simplex virus encephalitis in human UNC-93B deficiency.

Armanda Casrouge¹, Shen-Ying Zhang, Céline Eidenschenk

¹Laboratoire de Génétique Humaine des Maladies Infectieuses, Université de Paris René Descartes, INSERM, U550, Faculté de Médecine Necker, Paris 75015, France.

Science (New York, N.Y.)

|September 16, 2006

Summary

A genetic cause for Herpes simplex virus-1 (HSV-1) encephalitis (HSE) was found in two children with a deficiency in the UNC-93B protein, impairing antiviral responses. This discovery highlights a specific genetic immunodeficiency linked to severe viral infections.

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Area of Science:

Immunology
Virology
Genetics

Background:

Herpes simplex virus-1 (HSV-1) encephalitis (HSE) is a common neurological disorder in Western countries.
The precise reasons for HSE development in some individuals remain unknown, despite widespread HSV-1 infection.

Observation:

Two children with HSE were identified to have an autosomal recessive deficiency in the intracellular protein UNC-93B.
This deficiency led to impaired cellular responses to interferon-alpha/beta and interferon-lambda.

Findings:

A specific genetic etiology for HSE has been elucidated, linked to UNC-93B protein deficiency.
This single-gene immunodeficiency selectively affects antiviral responses without compromising immunity to other pathogens.

Implications:

HSE can arise from a specific monogenic disorder of immunity.
This finding broadens the understanding of primary immunodeficiencies and their link to severe infectious diseases.
Highlights the critical role of UNC-93B in antiviral defense against HSV-1.