CASE REPORT


Bimodal Temporal Distribution of Herpes Explains Resistant Cases to Oral Antiviral Agents



K.L. Gaishauser1, *C.G. Burkhart2, 3
1 Department of Medicine, University of Toledo College of Medicine, Toledo, OH, USA
2 Clinical Professor, University of Toledo College of Medicine, Toledo, OH, USA
3 Clinical Assistant Professor, Ohio University College of Osteopathic Medicine, Toledo, OH, USA


Article Metrics

CrossRef Citations:
0
Total Statistics:

Full-Text HTML Views: 991
Abstract HTML Views: 1011
PDF Downloads: 358
ePub Downloads: 284
Total Views/Downloads: 2644
Unique Statistics:

Full-Text HTML Views: 536
Abstract HTML Views: 508
PDF Downloads: 228
ePub Downloads: 172
Total Views/Downloads: 1444



© 2019 Gaishauser and Burkhart.

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.

* Address Correspondence to this author at the Department of Medicine, University of Toledo College of Medicine, 2534 W. Village Drive, Toledo, OH 43614; Tel: (330)-421-2393; E-mail: korina.gaishauser@rockets.utoledo.edu


Abstract

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.

Keywords: Herpes, Antiviral agents, HSV, Biomodal temporal, Antiviral agents, Mucous membranes.