Interferon is a crucial component of the human immune system's response to infection by herpes simplex virus type 1 (HSV-1), but how important a role it plays in determining the severity of disease and explaining why newborns are so much more susceptible to HSV-1 infection than adults remains unclear. A comprehensive review of the contribution of type I interferon (IFN) to controlling HSV-1 infection is presented in an article published in DNA and Cell Biology, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the DNA and Cell Biology website until May 19, 2017. In the article entitled "The Type I Interferon Response and Age-Dependent Susceptibility to Herpes Simplex Virus Infection," Daniel Giraldo, Douglas Wilcox, and Richard Longnecker, Northwestern University Feinberg School of Medicine, Chicago, IL, provide an in-depth look at the IFN response to HSV-1 infection. The authors examine the factors that may explain why newborns infected with HSV-1 are at greater risk for serious and potentially life-threatening diseases such as herpes simplex encephalitis, whereas in adults orolabial lesions are the more likely result of HSV-1 infection.
"HSV is ubiquitous and approximately 70% of the population is infected with this virus. It may maintain a life-long relationship with the host establishing latency and reappearing upon stress. This study is important because it gives us insight into the differences between infection of young hosts and older individuals," says Carol Shoshkes Reiss, PhD, Editor-in-Chief, of DNA and Cell Biology and Professor, Departments of Biology and Neural Science, and Global Public Health at New York University, NY. Research reported in this publication was supported by the National Institutes of Health under Award Numbers T32 AI060523, T32 GM008152, F30 AI116106, R01 CA021776, and R01 EY023977. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
http://online.liebertpub.com/doi/full/10.1089/dna.2017.3668
