Chemokines and Chemokine Receptors Critical to Host Resistance Following Genital Herpes Simplex Virus Type 2 (HSV-2) Infection

Manoj Thapa1, Daniel J.J. Carr*, 1, 2
1 Department of Microbiology, Immunology
2 Ophthalmology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma-73104, USA

© 2008 Thapa and Carr et al.;

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: 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 Ophthalmology, DMEI #415, The University of Oklahoma Health Sciences Center, 608 Stanton L Young Blvd., Oklahoma City, OK 73104, USA; Tel: 405-271-8784; Fax: 405-271-8781 E-mail:


HSV-2 is a highly successful human pathogen with a remarkable ability to elude immune detection or counter the innate and adaptive immune response through the production of viral-encoded proteins. In response to infection, resident cells secrete soluble factors including chemokines that mobilize and guide leukocytes including T and NK cells, neutrophils, and monocytes to sites of infection. While there is built-in redundancy within the system, chemokines signal through specific membrane-bound receptors that act as antennae detailing a chemical pathway that will provide a means to locate and eliminate the viral insult. Within the central nervous system (CNS), the temporal and spatial expression of chemokines relative to leukocyte mobilization in response to HSV-2 infection has not been elucidated. This paper will review some of the chemokine/chemokine receptor candidates that appear critical to the host in viral resistance and clearance from the CNS and peripheral tissue using murine models of genital HSV-2 infection.

Keywords: Genital HSV-2, Chemokines, Chemokine Receptors, Leukocytes, CNS.