The role of chemokines during herpes simplex virus-1 infection

Todd, RStephen

doi:10.2741/3045

Cited by 55 publications

(43 citation statements)

References 119 publications

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“…3 Furthermore, this process is initiated by the expression of several chemokines. Using endpoint PCR, early studies identified several chemokines that were induced following ocular HSV-1 infection including CXCL1, CXCL2, CXCL10, CCL2, and CCL4.…”

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confidence: 99%

CXCL1-Deficient Mice Are Highly Sensitive toPseudomonas aeruginosabut Not Herpes Simplex Virus Type 1 Corneal Infection

Bryant-Hudson

Carr²

2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To determine the role of the chemokine CXCL1 on leukocyte recruitment, cytokine production and host resistance during HSV-1 and Pseudomonas aeruginosa infection.METHODS. Viral titer and bacterial load were compared following infection of wild-type (WT) and CXCL1 À/À mice. Corneal leukocyte recruitment was determined using flow cytometry. Cytokine levels were assessed by luminex-based suspension arrays. Hematoxylin and eosin (H&E) staining, confocal microscopy, and optical coherence tomography (OCT) were used to visualize leukocyte recruitment and corneal thickening. RESULTS. HSV-1-infected WT and CXCL1À/À mice possessed similar viral titers in the cornea during late acute infection. Flow cytometry analysis detected similar leukocyte levels in the cornea following infection as well. By comparison, there was a significant increase in P. aeruginosa recovered from CXCL1 À/À corneas as compared with WT mice. Imaging analysis and histochemical staining revealed impaired leukocyte recruitment to the central cornea and earlier corneal thickening in CXCL1 À/À mice. IFN-c, CCL2, and CCL5 protein levels were similar between WT and CXCL1 À/À corneas following HSV-1 or P. aeruginosa infection. However, CXCL2 levels were significantly reduced in the CXCL1 À/À corneas following either infection.CONCLUSIONS. The absence of CXCL1 and CXCL2 expression significantly impairs the ability of the host to control P. aeruginosa replication through the recruitment of leukocytes to the central cornea. In contrast, CXCL1, CXCL2, and the cells they recruit, are not required for HSV-1 clearance during acute infection. (Invest Ophthalmol Vis Sci. 2012;53:6785-6792)

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confidence: 99%

CXCL1-Deficient Mice Are Highly Sensitive toPseudomonas aeruginosabut Not Herpes Simplex Virus Type 1 Corneal Infection

Bryant-Hudson

Carr²

2012

Invest. Ophthalmol. Vis. Sci.

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“…In comparison, a viral mimic such as poly I:C was capable of upregulating gIP, CXCd, CK1, CK3, CK5B, CK7A and CK12, therefore, the differences that may arise from the profile induced by poly I:C and that produced by the two viruses may give us an indication of alterations provoked specifically by the virus most probably in its benefit. These viral-induced alterations could be either up or down-modulations of one specific chemokine, as has been demonstrated in many different mammalian viral models [9,[36][37][38][39]. Preliminary studies performed in our group using eukaryotic expression vectors, revealed some immune effects of CK5B, CK6 and CK7A, previously catalogued as ''inducible'' CC chemokines [29].…”

Section: Discussionmentioning

confidence: 87%

Chemokine transcription in rainbow trout (Oncorhynchus mykiss) is differently modulated in response to viral hemorrhagic septicaemia virus (VHSV) or infectious pancreatic necrosis virus (IPNV)

Montero¹,

Chaves-Pozo²,

Cuesta³

et al. 2009

Fish & Shellfish Immunology

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“…The ultimate goal is to understand HSV-1 neurotropism, namely the predilection of the virus to infect and replicate in specific brain regions and cells. The ex vivo brain system, that has extensively been used in physiological studies of the central nervous system (Corner et al, 2005;House et al, 1998), lacks aspects of complete neuronal circuits and the immune response; both are known to be important factors in HSV encephalitis (Barnett et al, 1994;Conrady et al, 2010, Norgren & Lehman, 1998Wuest & Carr, 2008). This experimental system, on the other hand, with its normal tissue architecture, facilitated the study of factors, such as extra-cellular molecules, that affect virus-tissue interactions, and thus it complements previous in vivo and tissue culture studies.…”

Section: Discussionmentioning

confidence: 99%

Restrictions that control herpes simplex virus type 1 infection in mouse brain ex vivo

Cohen

Braun

Tsalenchuck

et al. 2011

Journal of General Virology

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Elucidating the cellular and molecular factors governing herpes simplex virus type 1 (HSV-1) neurotropism is a prerequisite for understanding HSV-1 encephalitis and for targeting HSV-1-derived vectors for gene transfer to the brain. Earlier we had described an ex vivo system of mouse brain slices and demonstrated a selective and unique infection pattern, mostly around the ventricles. Here, we examined tissue factors controlling HSV-1 infection of brain slices. We demonstrated that heparan sulphate, while an important factor, does not determine the infection pattern. Hyaluronic acid, but not collagen, appears to enhance HSV-1 brain infection. To investigate whether tissue distribution of viral receptors determines the infection pattern, we examined transcription of herpes virus entry mediator and nectin-1 receptor genes in infected and uninfected brain regions. Both the infected and the uninfected regions express the receptors. We also explored the influence of intra-cellular factors. HSV-1 does not preferentially infect proliferating cells in the brain slices, despite its predilection to the ventricular zones. To delineate the step at which the HSV-1 infection cascade is restricted, mRNA was isolated following tissue infection, and transcription of the immediate-early and late viral genes was evaluated. The results indicated that HSV-1 genes are not expressed in regions that do not express a viral reporter gene. Therefore, we conclude that tissue resistance to infection is associated with a block at or prior to the immediate-early mRNA synthesis. Taken together, using the ex vivo system of organotypic culture we describe here extra-cellular and intra-cellular restriction levels of HSV-1 brain infection.

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The role of chemokines during herpes simplex virus-1 infection

Cited by 55 publications

References 119 publications

CXCL1-Deficient Mice Are Highly Sensitive toPseudomonas aeruginosabut Not Herpes Simplex Virus Type 1 Corneal Infection

CXCL1-Deficient Mice Are Highly Sensitive toPseudomonas aeruginosabut Not Herpes Simplex Virus Type 1 Corneal Infection

Chemokine transcription in rainbow trout (Oncorhynchus mykiss) is differently modulated in response to viral hemorrhagic septicaemia virus (VHSV) or infectious pancreatic necrosis virus (IPNV)

Restrictions that control herpes simplex virus type 1 infection in mouse brain ex vivo

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