Low-molecular weight mannogalactofucans prevent herpes simplex virus type 1 infection via activation of Toll-like receptor 2

Abstract Natural interferon-producing cells (IPCs) specialize in the production of high levels of type 1 interferons (IFNs) in response to encapsulated DNA and RNA viruses. Here we demonstrate that the secretion of type 1 IFN in response to herpes simplex virus type 1 (HSV-1) in vitro is mediated by the toll-like receptor 9 (TLR9)/MyD88 pathway. Moreover, IPCs produce interleukin-12 (IL-12) in response to HSV-1 in vitro, which is also dependent on TLR9/ MyD88 signaling. Remarkably, though TLR9/MyD88-deficiency abrogates IPC responses to HSV-1 in vitro, mice lacking either MyD88 or TLR9 are capable of controlling HSV-1 replication in vivo after local infection, demonstrating that TLR9- and MyD88-independent pathways in cells other than IPCs can effectively compensate for defective IPC responses to HSV-1.

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Isolation and characterization of a large molecular-weight polypeptide of herpes simplex virus type 1

Virology ◽

10.1016/0042-6822(74)90414-0 ◽

1974 ◽

Vol 62 (2) ◽

pp. 539-551 ◽

Cited By ~ 52

Author(s):

Richard J. Courtney ◽

Matilda Benyesh-Melnick

Keyword(s):

Molecular Weight ◽

Herpes Simplex Virus ◽

Herpes Simplex ◽

Virus Type ◽

Herpes Simplex Virus Type ◽

Isolation And Characterization ◽

Large Molecular Weight ◽

Simplex Virus

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Nuclear processing of viral high-molecular-weight RNA in cells infected with herpes simplex virus type 1.

Journal of Virology ◽

10.1128/jvi.35.2.382-389.1980 ◽

1980 ◽

Vol 35 (2) ◽

pp. 382-389 ◽

Cited By ~ 6

Author(s):

B Jacquemont ◽

A Garcia ◽

J Huppert

Keyword(s):

Molecular Weight ◽

Herpes Simplex Virus ◽

Herpes Simplex ◽

High Molecular Weight ◽

Virus Type ◽

Herpes Simplex Virus Type ◽

Simplex Virus ◽

Nuclear Processing ◽

In Cells

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Effects of toll-like receptor 3 on herpes simplex virus type-1-infected mouse neural stem cells

Canadian Journal of Microbiology ◽

10.1139/cjm-2014-0540 ◽

2015 ◽

Vol 61 (3) ◽

pp. 201-208 ◽

Cited By ~ 5

Author(s):

Xiuning Sun ◽

Lihong Shi ◽

Haoyun Zhang ◽

Ruifang Li ◽

Ruiwen Liang ◽

...

Keyword(s):

Stem Cells ◽

Herpes Simplex Virus ◽

Herpes Simplex ◽

Neural Stem Cells ◽

Virus Type ◽

Herpes Simplex Virus Type ◽

Toll Like Receptor ◽

Simplex Virus ◽

Hsv 1

In this study, we aimed to investigate the effect of herpes simplex virus type-1 (HSV-1) infection on the phosphorylation of interferon regulatory factor 3 (IRF3) and the expression of interferon-β (IFN-β), as well as to clarify the functions of toll-like receptor 3 (TLR3) in mouse neural stem cells (NSCs) infected with HSV-1. In HSV-1-infected cultured NSCs, immunofluorescence, reverse transcription – polymerase chain reaction, Western blot, and ELISA were performed to reveal the expression patterns of TLR3, IRF3, and IFN-β. Then, lentivirus-mediated RNA interference (RNAi) was used to block the expression of TLR3, and its effect on host resistance to HSV-1 infection was investigated. Under uninfected conditions, NSCs expressed TLR3 and phosphorylated IRF3, but after infection, the expression level of TLR3 was upregulated and the phosphorylation level of IRF3 in the nucleus was significantly enhanced, while IFN-β was also expressed. After TLR3 expression was blocked by lentivirus-mediated RNAi, IRF3 phosphorylation and IFN-β expression were downregulated. Therefore, HSV-1 upregulated the expression of TLR3 in NSCs and promoted nuclear translocation after IRF3 was phosphorylated to induce IFN-β expression. TLR3 exhibited an anti-HSV-1 infection capacity via innate immune functions.

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