scholarly journals Innate Recognition Network Driving Herpes Simplex Virus-Induced Corneal Immunopathology: Role of the Toll Pathway in Early Inflammatory Events in Stromal Keratitis

2007 ◽  
Vol 81 (20) ◽  
pp. 11128-11138 ◽  
Author(s):  
Pranita P. Sarangi ◽  
Bumseok Kim ◽  
Evelyn Kurt-Jones ◽  
Barry T. Rouse
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Early Recognition ◽  
Subsequent Development ◽  
Inflammatory Lesion ◽  
Recognition System ◽  
Ocular Infection ◽  
Stromal Keratitis ◽  
Simplex Virus

ABSTRACT Ocular infection with herpes simplex virus (HSV) sets off an array of events that succeed in clearing virus from the cornea but leaves the tissue with a CD4+ T-cell-orchestrated chronic inflammatory lesion that impairs vision. We demonstrate that Toll-like receptor (TLR) signaling forms a part of the recognition system that induces the syndrome that eventually culminates in immunopathology. Accordingly, in a comparison of the outcomes of infection in wild-type (WT) mice and those lacking TLR function, it was apparent that the absence of TLR2 and, to a lesser extent, TLR9 resulted in significantly diminished lesions. Similarly, mice lacking the adapter molecule MyD88 were resistant to lesion development, but such animals were also unable to control infection, with most succumbing to lethal encephalitis. The susceptibility of TLR4−/− animals was also evaluated. These animals developed lesions, which were more severe, more rapidly than did WT animals. We discuss the possible mechanisms by which early recognition of HSV constituents impacts the subsequent development of immunopathological lesions.

scholarly journals The role of natural killer cells in the development of herpes simplex virus type 1 induced stromal keratitis in mice

Eye ◽  
1994 ◽  
Vol 8 (3) ◽  
pp. 298-306 ◽  
Author(s):  
Richard R Tamesis ◽  
Elisabeth M Messmer ◽  
Beverly A Rice ◽  
James E Dutt ◽  
C Stephen Foster
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Stromal Keratitis ◽  
Simplex Virus

scholarly journals Role of Intravenous Acyclovir in Treatment of Herpes Simplex Virus Stromal Keratitis with Ulceration: A Review of 2 Cases

2021 ◽  
Vol 22 ◽  
Author(s):  
Punyanuch Pisitpayat ◽  
Passara Jongkhajornpong ◽  
Kaevalin Lekhanont ◽  
Manachai Nonpassopon
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Intravenous Acyclovir ◽  
Stromal Keratitis ◽  
Simplex Virus

scholarly journals Herpes Simplex Virus-Induced Keratitis: Evaluation of the Role of Molecular Mimicry in Lesion Pathogenesis

2001 ◽  
Vol 75 (7) ◽  
pp. 3077-3088 ◽  
Author(s):  
Shilpa P. Deshpande ◽  
Sujin Lee ◽  
Mei Zheng ◽  
Byeongwoon Song ◽  
David Knipe ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Molecular Mimicry ◽  
T Cell Response ◽  
Activation Mechanism ◽  
Mouse Strains ◽  
Ocular Infection ◽  
Simplex Virus

ABSTRACT Viruses are suspected but usually unproven triggering factors in autoimmunity. One favored mechanism to explain the role of viruses in the genesis of autoimmunity is molecular mimicry. An immunoinflammatory blinding lesion called herpetic stromal keratitis (HSK) that follows ocular infection with herpes simplex virus (HSV) is suggested to result from a CD4+ T-cell response to a UL6 peptide of HSV that cross-reacts with a corneal autopeptide shared with the immunoglobulin G2ab (IgG2ab) isotype. The present report reevaluates the molecular mimicry hypothesis to explain HSK pathogenesis. Our results failed to reveal cross-reactivity between the UL6 and IgG2ab peptides or between peptide reactive T cells and HSV antigens. More importantly, animals infected with HSV failed to develop responses that reacted with either peptide, and infection with a recombinant vaccinia UL6 vector failed to cause HSK, in spite of generating UL6 reactivity. Other lines of evidence also failed to support the molecular mimicry hypothesis, such as the failure to affect HSK severity upon tolerization of susceptible BALB/c and B-cell-deficient mice with IgG2ab or UL6 peptides. An additional study system revealed that HSK could be induced in mouse strains, such as the OT2 × RAG1−/− mice (T cell receptor transgenic recognizing OVA323–339) that were unable to produce CD4+ T-cell responses to any detectable HSV antigens. Our results cast doubt on the molecular mimicry hypothesis as an explanation for the pathogenesis of HSK and indicate that if autoimmunity is involved its likely proceeds via a bystander activation mechanism.

scholarly journals Herpes simplex virus-induced stromal keratitis: role of T-lymphocyte subsets in immunopathology.

1989 ◽  
Vol 63 (2) ◽  
pp. 769-775 ◽  
Author(s):  
C K Newell ◽  
S Martin ◽  
D Sendele ◽  
C M Mercadal ◽  
B T Rouse
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Lymphocyte ◽  
Lymphocyte Subsets ◽  
T Lymphocyte Subsets ◽  
Stromal Keratitis ◽  
Simplex Virus

scholarly journals Roles of Us8A and Its Phosphorylation Mediated by Us3 in Herpes Simplex Virus 1 Pathogenesis

2016 ◽  
Vol 90 (12) ◽  
pp. 5622-5635 ◽  
Author(s):  
Akihisa Kato ◽  
Tomoko Ando ◽  
Shinya Oda ◽  
Mizuki Watanabe ◽  
Naoto Koyanagi ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Ocular Infection ◽  
Null Mutant ◽  
Herpes Simplex Virus 1 ◽  
The Central Nervous System ◽  
Infected Cells ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTThe herpes simplex virus 1 (HSV-1) Us8A gene overlaps the gene that encodes glycoprotein E (gE). Previous studies have investigated the roles of Us8A in HSV-1 infection using null mutations in Us8A and gE; therefore, the role of Us8A remains to be elucidated. In this study, we investigated the function of Us8A and its phosphorylation at serine 61 (Ser-61), which we recently identified as a phosphorylation site by mass spectrometry-based phosphoproteomic analysis of HSV-1-infected cells, in HSV-1 pathogenesis. We observed that (i) the phosphorylation of Us8A Ser-61 in infected cells was dependent on the activity of the virus-encoded Us3 protein kinase; (ii) the Us8A null mutant virus exhibited a 10-fold increase in the 50% lethal dose for virulence in the central nervous system (CNS) of mice following intracranial infection compared with a repaired virus; (iii) replacement of Ser-61 with alanine (S61A) in Us8A had little effect on virulence in the CNS of mice following intracranial infection, whereas it significantly reduced the mortality of mice following ocular infection to levels similar to the Us8A null mutant virus; (iv) the Us8A S61A mutation also significantly reduced viral yields in mice following ocular infection, mainly in the trigeminal ganglia and brains; and (v) a phosphomimetic mutation at Us8A Ser-61 restored wild-type viral yields and virulence. Collectively, these results indicate that Us8A is a novel HSV-1 virulence factor and suggest that the Us3-mediated phosphorylation of Us8A Ser-61 regulates Us8A function for viral invasion into the CNS from peripheral sites.IMPORTANCEThe DNA genomes of viruses within the subfamilyAlphaherpesvirinaeare divided into unique long (UL) and unique short (Us) regions. Us regions contain alphaherpesvirus-specific genes. Recently, high-throughput sequencing of ocular isolates of HSV-1 showed that Us8A was the most highly conserved of 13 herpes simplex virus 1 (HSV-1) genes mapped to the Us region, suggesting Us8A may have an important role in the HSV-1 life cycle. However, the specific role of Us8A in HSV-1 infection remains to be elucidated. Here, we show that Us8A is a virulence factor for HSV-1 infection in mice, and the function of Us8A for viral invasion into the central nervous system from peripheral sites is regulated by Us3-mediated phosphorylation of the protein at Ser-61. This is the first study to report the significance of Us8A and its regulation in HSV-1 infection.

scholarly journals Role of miR-132 in Angiogenesis after Ocular Infection with Herpes Simplex Virus

2012 ◽  
Vol 181 (2) ◽  
pp. 525-534 ◽  
Author(s):  
Sachin Mulik ◽  
John Xu ◽  
Pradeep B.J. Reddy ◽  
Naveen K. Rajasagi ◽  
Fernanda Gimenez ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Ocular Infection ◽  
Simplex Virus

scholarly journals Gamma Interferon Impedes the Establishment of Herpes Simplex Virus Type 1 Latent Infection but Has No Impact on Its Maintenance or Reactivation in Mice

2000 ◽  
Vol 74 (14) ◽  
pp. 6680-6683 ◽  
Author(s):  
Julie A. Lekstrom-Himes ◽  
Rona A. LeBlanc ◽  
Lesley Pesnicak ◽  
Matthew Godleski ◽  
Stephen E. Straus
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Gamma Interferon ◽  
Viral Reactivation ◽  
Ocular Infection ◽  
Virus Reactivation ◽  
Ifn Γ ◽  
Simplex Virus

ABSTRACT Murine models of gamma interferon (IFN-γ) deficiency demonstrate the role of this cytokine in attenuating acute herpes simplex virus (HSV) disease; however, the effect of IFN-γ on the establishment and maintenance of neuronal latency and viral reactivation is not known. Using the IFN-γ knockout (GKO) model of IFN-γ deficiency and sensitive quantitative PCR methods, we show that IFN-γ significantly reduces the ganglion content of latent HSV-1 in BALB/c mice, which in turn delays viral time to reactivation following UV irradiation. Similar effects were not seen in the C57BL/6 strain. These results indicate that IFN-γ significantly attenuates latent HSV infection in the mouse model of ocular infection but has no impact on the maintenance of latency or virus reactivation.

Role of herpes simplex virus type 1 (HSV-1) in the pathogenesis of peptic ulcer disease

2001 ◽  
Vol 120 (5) ◽  
pp. A136-A137
Author(s):  
K TSAMAKIDES ◽  
E PANOTOPOULOU ◽  
D DIMITROULOPOULOS ◽  
M CHRISTOPOULO ◽  
D XINOPOULOS ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Peptic Ulcer Disease ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Ulcer Disease ◽  
Simplex Virus
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