scholarly journals Immunological Aspects of Acute and Recurrent Herpes Simplex Keratitis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jacek Rolinski ◽  
Iwona Hus
Keyword(s):  
Herpes Simplex ◽  
Current Knowledge ◽  
Ocular Infection ◽  
Corneal Scarring ◽  
Recurrent Herpes ◽  
Chronic Inflammatory Reaction ◽  
Herpes Simplex Keratitis ◽  
Methods Of Treatment ◽  
Therapeutical Options

Herpes simplex keratitis (HSK) belongs to the major causes of visual morbidity worldwide and available methods of treatment remain unsatisfactory. Primary infection occurs usually early in life and is often asymptomatic. Chronic visual impairment and visual loss are caused by corneal scaring, thinning, and vascularization connected with recurrent HSV infections. The pathogenesis of herpetic keratitis is complex and is still not fully understood. According to the current knowledge, corneal scarring and vascularization are the result of chronic inflammatory reaction against HSV antigens. In this review we discuss the role of innate and adaptive immunities in acute and recurrent HSV ocular infection and present the potential future targets for novel therapeutical options based on immune interventions.

scholarly journals IL28B Genetic Variations in Patients with Recurrent Herpes Simplex Keratitis

Medicina ◽  
2019 ◽  
Vol 55 (10) ◽  
pp. 642 ◽  
Author(s):  
Savić Borivoje ◽  
Stanojlović Svetlana ◽  
Hadži-Milić Milan ◽  
Đonović Nela ◽  
Milošević-Đorđević Olivera ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Il28b Genotype ◽  
Host Genotype ◽  
Nerve Branch ◽  
Corneal Scarring ◽  
Viral Shedding ◽  
Recurrent Herpes ◽  
History Of ◽  
Herpes Simplex Keratitis ◽  
Hsv 1

Background and objectives: Recurrent herpes simplex keratitis (HSK) is the most common cause of corneal blindness in the developed world. A relationship between host gene polymorphisms and the recurrence of herpes simplex virus (HSV) infection has previously been proposed. Thus, the aim of this study was to investigate a potential association between the IL28B host genotype and recurrent HSK. Materials and Methods: Eighty patients older than 18 years of age of both genders with a history of recurrent herpes simplex labialis (HSL) were considered for inclusion. Seventy-five of these patients were found to be seropositive for HSV-1 and were subsequently enrolled in the study. Twenty-four of the enrolled patients also had a history of recurrent HSK associated with severe corneal scarring and visual acuity deterioration. Total DNA was isolated from whole blood samples. A single-nucleotide polymorphism (SNP) rs12979860 near the IL28B gene on chromosome 19 was genotyped. Results: A significant association was observed between recurrent HSK and two SNPs of the IL28B genotype (CCrs12979860 and CTrs12979860, p < 0.01). The variation CCrs12979860 showed a significantly greater association with HSK (16 out of 26 patients) compared with CTrs12979860 (8 out of 34 patients). Conclusion: Seropositive individuals with a history of recurrent HSK are likely to have the CC IL28B genotype. This genotype may be related to incomplete control of the infection and more frequent periodical viral shedding along the first nerve branch of the trigeminal ganglion, which clinically manifests as recurrent herpes keratitis. The clinical manifestation of recurrent HSV-1 infection seems to be influenced by polymorphism of the IL28B genotype.

scholarly journals The Role of Tissue Resident Memory CD4 T Cells in Herpes Simplex Viral and HIV Infection

2020 ◽  
Author(s):  
Thomas Ray O'Neil ◽  
Kevin Hu ◽  
Naomi Truong ◽  
Sana Arshad ◽  
Barbara Shacklett ◽  
...  
Keyword(s):  
T Cells ◽  
Herpes Simplex ◽  
Cd4 T Cells ◽  
Sexual Transmission ◽  
Trigeminal Ganglia ◽  
Hiv Replication ◽  
Recurrent Herpes ◽  
Resident Memory T Cells ◽  
Memory Cd4 T Cells

Tissue resident memory T cells (TRM) were first described in 2009. While initially the major focus was on CD8 TRM, there has been recently an increased interest in defining the phenotype and the role of CD4 TRM in diseases. Circulating CD4 T cells seed tissue CD4 TRM, but there also appears to be an equilibrium between CD4 TRM and blood CD4 T cells. CD4 TRM are more mobile than CD8 TRM, usually localized deeper within the dermis/lamina propria and yet may exhibit synergy with CD8 TRM in disease control. This has been demonstrated in herpes simplex infections in mice. In human recurrent herpes infections, both CD4 and CD8 TRM persisting between lesions may control asymptomatic shedding through interferon gamma secretion, although this has been more clearly shown for CD8 T cells. The exact role of the CD4/CD8 TRM axis in the trigeminal ganglia and/or cornea in controlling recurrent herpetic keratitis is unknown. In HIV, CD4 TRM have now been shown to be a major target for productive and latent infection in cervix. In HSV and HIV co-infections, CD4 TRM persisting in the dermis support HIV replication. Further understanding of the role of CD4 TRM and their induction by vaccines may help control sexual transmission by both viruses.

scholarly journals Clinical Efficacy of Oral Ganciclovir for Prophylaxis and Treatment of Recurrent Herpes Simplex Keratitis

2015 ◽  
Vol 128 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Xin Wang ◽  
Linnong Wang ◽  
Nianlang Wu ◽  
Xinjun Ma ◽  
Jianjiang Xu
Keyword(s):  
Herpes Simplex ◽  
Clinical Efficacy ◽  
Oral Ganciclovir ◽  
Recurrent Herpes ◽  
Herpes Simplex Keratitis

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.

Recurrent Herpes Simplex Keratitis Adjacent to Femtosecond Laser Arcuate Keratotomies

2013 ◽  
Vol 131 (10) ◽  
pp. 1372 ◽  
Author(s):  
Nathaniel Nataneli ◽  
Jean S. M. Chai ◽  
Eric D. Donnenfeld ◽  
Henry D. Perry
Keyword(s):  
Herpes Simplex ◽  
Femtosecond Laser ◽  
Recurrent Herpes ◽  
Herpes Simplex Keratitis
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