Bimodal Temporal Distribution of Herpes Explains Resistant Cases to Oral Antiviral Agents
K.L. Gaishauser1, *C.G. Burkhart2, 3
Identifiers and Pagination:Year: 2019
First Page: 1
Last Page: 2
Publisher Id: TODJ-13-1
Article History:Received Date: 28/06/2018
Revision Received Date: 20/12/2018
Acceptance Date: 14/01/2019
Electronic publication date: 31/1/2019
Collection year: 2019
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Herpes Simplex Virus (HSV) is a double-stranded virus that affects the skin and mucous membranes. There has been a long-standing dogma stating that the virus remains dormant and is reactivated from the dorsal root ganglia. However, more recent studies have established that there is a secondary mode of viral reactivation from the epidermis itself. These two distinct reactivation patterns help explain why prophylactic antivirals do not consistently prevent herpes outbreaks.