title: 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 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.
authors.affiliation: Department of Microbiology, Department of Pediatrics, The Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA Dusan.Bogunovic@mssm.edu.
authors.forename: Dusan
authors.initials: D
authors.lastname: Bogunovic
mesh_terms: D000328:Adult; D000998:Antiviral Agents; D002648:Child; D020803:Encephalitis, Herpes Simplex / Q000276:immunology*; D006561:Herpes Simplex / Q000276:immunology*; D018259:Herpesvirus 1, Human / Q000276:immunology*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007370:Interferon Type I / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D017471:Receptors, Interferon / Q000378:metabolism; D015398:Signal Transduction; D014779:Virus Replication
chemical_list: D000998:Antiviral Agents; D007370:Interferon Type I; D017471:Receptors, Interferon