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
Identifiers and Pagination:Year: 2008
First Page: 33
Last Page: 41
Publisher Id: TOIJ-1-33
Article History:Received Date: 3/03/2008
Revision Received Date: 17/04/2008
Acceptance Date: 2/05/2008
Electronic publication date: 20/5/2008
Collection year: 2008
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.
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.