The role of toll-like receptor ligands/agonists in protection against genital HSV-2 infection

被引:29
作者
Gill, Navkiran [1 ]
Davies, Elizabeth J. [1 ]
Ashkar, Ali A. [1 ]
机构
[1] McMaster Univ, Hlth Sci Ctr, Ctr Gene Therapeut, Dept Pathol & Mol Med, Hamilton, ON L8N 3ZS, Canada
关键词
HSV-2; innate antiviral; mucosal; TLRs;
D O I
10.1111/j.1600-0897.2007.00558.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Control of virus replication initially depends on rapid activation of the innate immune responses. Toll-like receptor (TLR) ligands are potent inducers of innate immunity against viral infections, including herpes simplex virus (HSV). HSV-2 is currently one of the most common sexually transmitted infections in developed nations and is becoming more prevalent in adolescents. HSV-2 infects the genital mucosa and is associated with an increased risk of obtaining other sexually transmitted infections such as HIV. There is currently no vaccine available against HSV-2. In the last several years, there has been an interest in utilizing Toll-like receptor (TLR) ligands to initiate innate immune responses in order to provide an early line of defence against viral replication. This review highlights recent studies investigating the effect of various TLR ligands on genital HSV-2 infection. A considerable body of information has been published on the effect of local delivery of TLR ligands on HSV-2 replication in genital mucosa. We have outlined ligands that have a potential to provide protection against HSV-2 infection. In addition, we have presented possible mechanisms by which the local delivery of TLR ligands provides innate protection against genital HSV-2.
引用
收藏
页码:35 / 43
页数:9
相关论文
共 52 条
[1]   Toll-like receptors in the induction of the innate immune response [J].
Aderem, A ;
Ulevitch, RJ .
NATURE, 2000, 406 (6797) :782-787
[2]   Toll-like receptors: critical proteins linking innate and acquired immunity [J].
Akira, S ;
Takeda, K ;
Kaisho, T .
NATURE IMMUNOLOGY, 2001, 2 (08) :675-680
[3]   Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].
Alexopoulou, L ;
Holt, AC ;
Medzhitov, R ;
Flavell, RA .
NATURE, 2001, 413 (6857) :732-738
[4]  
[Anonymous], 1996, Fields virology
[5]   Toll-like receptor (TLR)-3, but not TLR4, agonist protects against genital herpes infection in the absence of inflammation seen with CpG DNA [J].
Ashkar, AA ;
Yao, XD ;
Gill, N ;
Sajic, D ;
Patrick, AJ ;
Rosenthal, KL ;
Rosenthal, L .
JOURNAL OF INFECTIOUS DISEASES, 2004, 190 (10) :1841-1849
[6]   CpG DNA stimulates autoreactive immature B cells in the bone marrow [J].
Azulay-Debby, Hilla ;
Edry, Efrat ;
Melamed, Doron .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2007, 37 (06) :1463-1475
[7]   Daily or weekly therapy with resiquimod (R-848) reduces genital recurrences in herpes simplex virus-infected guinea pigs during and after treatment [J].
Bernstein, DI ;
Harrison, CJ ;
Tomai, MA ;
Miller, RL .
JOURNAL OF INFECTIOUS DISEASES, 2001, 183 (06) :844-849
[8]   Toll-like receptor 3 mediates a more potent antiviral response than toll-like receptor 4 [J].
Doyle, SE ;
O'Connell, R ;
Vaidya, SA ;
Chow, EK ;
Yee, K ;
Cheng, GH .
JOURNAL OF IMMUNOLOGY, 2003, 170 (07) :3565-3571
[9]   IRF3 mediates a TLR3/TLR4-specific antiviral gene program [J].
Doyle, SE ;
Vaidya, SA ;
O'Connell, R ;
Dadgostar, H ;
Dempsey, PW ;
Wu, TT ;
Rao, G ;
Sun, R ;
Haberland, ME ;
Modlin, RL ;
Cheng, G .
IMMUNITY, 2002, 17 (03) :251-263
[10]   Characterization of Toll-like receptors in the female reproductive tract in humans [J].
Fazeli, A ;
Bruce, C ;
Anumba, DO .
HUMAN REPRODUCTION, 2005, 20 (05) :1372-1378