Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense

ABSTRACT In most children and adults, primary infection with herpes simplex virus 1 (HSV-1) is asymptomatic. However, very rarely (incidence of 1 in 1,000,000), it can cause herpes simplex encephalitis (HSE). HSE also occurs in infants but with a much starker incidence of one in three. This age diff...

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Autor principal:	Dusan Bogunovic
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2016
Materias:	Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/96050b9a6dd94199896d0c95674d0d37
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spelling	oai:doaj.org-article:96050b9a6dd94199896d0c95674d0d372021-11-15T15:50:17ZType I Interferons in Newborns—Neurotoxicity versus Antiviral Defense10.1128/mBio.00639-162150-7511https://doaj.org/article/96050b9a6dd94199896d0c95674d0d372016-07-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00639-16https://doaj.org/toc/2150-7511ABSTRACT In most children and adults, primary infection with herpes simplex virus 1 (HSV-1) is asymptomatic. However, very rarely (incidence of 1 in 1,000,000), it can cause herpes simplex encephalitis (HSE). HSE also occurs in infants but with a much starker incidence of one in three. This age difference in susceptibility to HSV-1-caused HSE is not well understood. In a recent article in mBio, authors have identified the choroid plexus as the anatomical site of robust HSV-1 replication in the brain. They point to low levels of type I interferon (IFN) receptor as causal of the lack of HSV-1 replication control in neonates, in contrast to adults. Here, I discuss these findings in the context of human genetic evidence. I point to the balancing act of type I IFN acting as a neurotoxin and an antiviral agent, an evolutionary choice of a lesser evil.Dusan BogunovicAmerican Society for MicrobiologyarticleMicrobiologyQR1-502ENmBio, Vol 7, Iss 3 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	Microbiology QR1-502
spellingShingle	Microbiology QR1-502 Dusan Bogunovic Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense
description	ABSTRACT In most children and adults, primary infection with herpes simplex virus 1 (HSV-1) is asymptomatic. However, very rarely (incidence of 1 in 1,000,000), it can cause herpes simplex encephalitis (HSE). HSE also occurs in infants but with a much starker incidence of one in three. This age difference in susceptibility to HSV-1-caused HSE is not well understood. In a recent article in mBio, authors have identified the choroid plexus as the anatomical site of robust HSV-1 replication in the brain. They point to low levels of type I interferon (IFN) receptor as causal of the lack of HSV-1 replication control in neonates, in contrast to adults. Here, I discuss these findings in the context of human genetic evidence. I point to the balancing act of type I IFN acting as a neurotoxin and an antiviral agent, an evolutionary choice of a lesser evil.
format	article
author	Dusan Bogunovic
author_facet	Dusan Bogunovic
author_sort	Dusan Bogunovic
title	Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense
title_short	Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense
title_full	Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense
title_fullStr	Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense
title_full_unstemmed	Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense
title_sort	type i interferons in newborns—neurotoxicity versus antiviral defense
publisher	American Society for Microbiology
publishDate	2016
url	https://doaj.org/article/96050b9a6dd94199896d0c95674d0d37
work_keys_str_mv	AT dusanbogunovic typeiinterferonsinnewbornsneurotoxicityversusantiviraldefense
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Type I Interferons in Newborns—Neurotoxicity versus Antiviral Defense

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