Alteration of intracerebral cytokine production in mice infected with herpes simplex virus types 1 and 2

Lewandowski, Gail; Hobbs, Monte V.; Bloom, Floyd E.

doi:10.1016/0165-5728(94)90143-0

Cited by 37 publications

(13 citation statements)

References 64 publications

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“…Their critical role in genital HSV-2 infection can well be anticipated, and studies have provided evidence of chemokine and pro-inflammatory cytokine production in the CNS following infection with 31,45,46,47]. However, most of the studies have focused on the mobilization of T and B cells into the vagina or mobilization of cells between vaginal epithelium and the draining lymph nodes during infection.…”

Section: Chemokines In the Cns During Hsv-2 Infectionmentioning

confidence: 99%

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

Thapa¹,

Carr²

2008

TOIJ

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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 membranebound 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. KeywordsGenital HSV-2; chemokines; chemokine receptors; leukocytes; CNS HSV-2 BIOLOGYHSV-2 is a large (150-200nm) double-stranded, DNA virus and a member of the subfamily α-Herpesviridae [1,2]. A mature virus contains a core, an icosahedral capsid, a tegument in which additional viral proteins reside, and an outer envelope [1]. An approximately 150,000 base pair linear DNA is packaged inside the capsid that encodes at least 80 different viral genes [1]. The outer membrane envelope contains viral glycoproteins (e.g. gB, gC, gD and heterodimer gH/gL) involved in a multistep viral entry into the target cell [3,4]. The viral entry begins with interaction of gB and gC to heparin sulfate proteoglycans present on the surface of target cells followed by gD binding to other surface receptors including herpes virus entry mediator A and nectin-1α [2,4]. The viral envelope subsequently fuses with the target cell membrane which requires gD, gB and the heterodimer gH/gL [2]. Following viral entry, local replication commences with a sequential cascade of viral lytic gene transcription/translation and subsequent packaging of unit length viral DNA into empty viral capsids [5,6,7]. The capsid then acquires viral tegument and glycoproteins followed by the envelopment of the capsid on the underside of the nuclear membrane [6]. After successful packaging of infectious virions, the virus is released thru the rupture of the cell membrane where it will enter sensory nerve endings in the basal aspect of epithelium and via retrograde transport traffic to sacral ganglia in the CNS [7,8]. One of the hallmark features of HSV-2 is the establishment of latency in a subpopulation of neurons following acute infection of sensory ganglia [9,10]. In normal adults, it can cause recurrent infection at the original portal of entry as well as adjacent sites after reactivation [11]. HSV-2 INFECTION OF THE CNSHSV-2 is one of the most common causes of genital ulcer disease in humans that can result in fatal encephalitis and meningitis...

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Section: Chemokines In the Cns During Hsv-2 Infectionmentioning

confidence: 99%

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

Thapa¹,

Carr²

2008

TOIJ

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“…One study comparing HSV-1 to HSV-2 and the immune responses at specific anatomical sites reported that ocular challenge of mice with HSV-1 (strain F) elicited a robust expression of several cytokines, including interleukin-1 alpha (IL-1␣), gamma IFN (IFN-␥), tumor necrosis factor alpha (TNF-␣), and IL-6, in the brain, whereas ocular infection with an unknown strain of HSV-2 resulted in a reduction in the cytokine signature (19). However, a caveat to this observation was that there was a 10-fold reduction in the HSV-2 challenge employed to infect mice compared to the HSV-1 challenge applied to the eye.…”

mentioning

confidence: 99%

Comparison of the Host Immune Response to Herpes Simplex Virus 1 (HSV-1) and HSV-2 at Two Different Mucosal Sites

Zheng

Conrady

Ward

et al. 2012

J Virol

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A study was undertaken to compare the host immune responses to herpes simplex virus 1 (HSV-1) and HSV-2 infection by the ocular or genital route in mice. Titers of HSV-2 from tissue samples were elevated regardless of the route of infection. The elevation in titers of HSV-2, including cell infiltration and cytokine/chemokine levels in the central nervous system relative to those found following HSV-1 infection, was correlative with inflammation. These results underscore a dichotomy between the host immune responses to closely related alphaherpesviruses.

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“…This phenomenon of altering the distribution and trafficking of class II is evident in the developmental regulation of surface MHC class II expression in dendritic cells, where during maturation, class II dramatically redistributes from intracellular lysosomal compartments to the cell surface (60,(72)(73)(74)(75). Moreover, HSV type 2 may use a similar mechanism of disrupting MHC class II trafficking as HCMV: it induces cytoplasmic and nuclear sequestering of MHC class II Ags in vivo, a phenomenon associated with lethal infection in the brains of mice (76,77).…”

Section: Discussionmentioning

confidence: 99%

Human Cytomegalovirus Disrupts Constitutive MHC Class II Expression

Cebulla

Miller

Zhang

et al. 2002

The Journal of Immunology

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CD8+ and CD4+ T lymphocytes are important in controlling human CMV (HCMV) infection, but the virus has evolved protean mechanisms to inhibit MHC-based Ag presentation and escape T lymphocyte immunosurveillance. Herein, the interaction of HCMV with the MHC class II Ag presentation pathway was investigated in cells stably transfected with class II transactivator. Flow cytometry experiments demonstrate that HCMV infection decreases cell-surface MHC class II expression. HCMV down-regulates MHC class II surface expression without a significant effect on class II RNA or steady-state protein levels. SDS-stability and confocal microscopy experiments demonstrate normal levels of steady-state peptide-loaded class II molecules in infected cells and that class II molecules reach late endosomal and HLA-DM positive peptide-loading compartments. However, MHC class II positive vesicles are retained in an abnormal perinuclear distribution. Finally, experiments with a mutant HCMV strain demonstrate that this novel mechanism of decreased MHC class II expression is not mediated by one of the known HCMV immunomodulatory genes. These defects in MHC class II expression combined with previously identified CMV strategies for decreasing MHC class I expression enables infected cells to evade T lymphocyte immunosurveillance.

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Alteration of intracerebral cytokine production in mice infected with herpes simplex virus types 1 and 2

Cited by 37 publications

References 64 publications

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

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

Comparison of the Host Immune Response to Herpes Simplex Virus 1 (HSV-1) and HSV-2 at Two Different Mucosal Sites

Human Cytomegalovirus Disrupts Constitutive MHC Class II Expression

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