Long-term outcomes of the Boston type I keratoprosthesis in eyes with previous herpes simplex virus keratitis

2017 ◽  
Vol 102 (1) ◽  
pp. 48-53 ◽  
Author(s):  
Melinda Fry ◽  
Carolina Aravena ◽  
Fei Yu ◽  
Jaffer Kattan ◽  
Anthony J Aldave
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Failure Rate ◽  
Cystoid Macular Oedema ◽  
Type I ◽  
Long Term Outcomes ◽  
Significant Difference ◽  
Simplex Virus ◽  
Boston Type I Keratoprosthesis

PurposeTo report the long-term outcomes of the Boston type I keratoprosthesis (Kpro) in eyes with prior herpes simplex virus (HSV) keratitis.MethodsRetrospective review of all Kpro procedures performed by a single surgeon from 1 May 2004 to 1 January 2015.Results13 of 173 Kpro procedures were performed in 11 eyes with prior HSV keratitis. There was not a significant difference in the percentage of eyes with and without prior HSV keratitis with preoperative (9% vs 8%, p=1.00) or postoperative (57% vs 60%, p=1.00) corrected distance visual acuity (CDVA) ≥20/200 or in the percentage of contralateral eyes with preoperative CDVA ≥20/50 (55% vs 30%, p=0.18). While several postoperative complications occurred approximately twice as often in eyes with prior HSV keratitis, including persistent epithelial defect (63.6% vs 34.1%; p=0.10), corneal infiltrate (27.3% vs 12.3%; p=0.17) and sterile vitritis (18.2% vs 9.4%; p=0.31), only cystoid macular oedema (45.5% vs 12.3%; p=0.01) was significantly more common. Similarly, while the Kpro retention failure rate in eyes with prior HSV keratitis was twice than that in eyes without it (0.15 vs 0.07 per year), the difference was not statistically significant (p=0.09).ConclusionAs greater than half of patients with unilateral HSV keratitis undergoing Kpro implantation have CDVA ≥20/50 in the contralateral eye, and as the Kpro retention failure rate in eyes with prior HSV keratitis is twice than that in eyes without prior HSV keratitis, caution should be exercised when considering Kpro implantation in these patients.

scholarly journals Long-term Outcomes of Pediatric Penetrating Keratoplasty for Herpes Simplex Virus Keratitis

2017 ◽  
Vol 173 ◽  
pp. 139-144 ◽  
Author(s):  
Juan Carlos Serna-Ojeda ◽  
Denise Loya-Garcia ◽  
Alejandro Navas ◽  
Alejandro Lichtinger ◽  
Arturo Ramirez-Miranda ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Penetrating Keratoplasty ◽  
Long Term Outcomes ◽  
Simplex Virus

scholarly journals Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
David Shahnazaryan ◽  
Rana Khalil ◽  
Claire Wynne ◽  
Caroline A. Jefferies ◽  
Joan Ní Gabhann-Dromgoole ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Immune Responses ◽  
Tear Film ◽  
Cell Protein ◽  
Type I ◽  
Type I Ifn ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
Hsv 1

AbstractHerpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious blindness in the developed world. Following infection the virus is initially suspended in the tear film, where it encounters a multi-pronged immune response comprising enzymes, complement, immunoglobulins and crucially, a range of anti-viral and pro-inflammatory cytokines. However, given that HSV-1 can overcome innate immune responses to establish lifelong latency throughout a susceptible individual’s lifetime, there is significant interest in understanding the mechanisms employed by HSV-1 to downregulate the anti-viral type I interferon (IFN) mediated immune responses. This study aimed to investigate the interactions between infected cell protein (ICP)0 and key elements of the IFN pathway to identify possible novel targets that contribute to viral immune evasion. Reporter gene assays demonstrated the ability of ICP0 to inhibit type I IFN activity downstream of pathogen recognition receptors (PRRs) which are known to be involved in host antiviral defences. Further experiments identified interferon regulatory factor (IRF)7, a driver of type I IFN, as a potential target for ICP0. These findings increase our understanding of the pathogenesis of HSK and suggest IRF7 as a potential therapeutic target.

scholarly journals HCF1 and OCT2 Cooperate with EBNA1 To Enhance OriP-Dependent Transcription and Episome Maintenance of Latent Epstein-Barr Virus

2016 ◽  
Vol 90 (11) ◽  
pp. 5353-5367 ◽  
Author(s):  
Jayaraju Dheekollu ◽  
Andreas Wiedmer ◽  
Daniel Sentana-Lledo ◽  
Joel Cassel ◽  
Troy Messick ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Epstein Barr Virus ◽  
Histone H3 ◽  
Type I ◽  
Barr Virus ◽  
Cellular Factors ◽  
Epstein Barr ◽  
Simplex Virus

ABSTRACTEpstein-Barr virus (EBV) establishes latent infections as multicopy episomes with complex patterns of viral gene transcription and chromatin structure. The EBV origin of plasmid replication (OriP) has been implicated as a critical control element for viral transcription, as well as viral DNA replication and episome maintenance. Here, we examine cellular factors that bind OriP and regulate histone modification, transcription regulation, and episome maintenance. We found that OriP is enriched for histone H3 lysine 4 (H3K4) methylation in multiple cell types and latency types. Host cell factor 1 (HCF1), a component of the mixed-lineage leukemia (MLL) histone methyltransferase complex, and transcription factor OCT2 (octamer-binding transcription factor 2) bound cooperatively with EBNA1 (Epstein-Barr virus nuclear antigen 1) at OriP. Depletion of OCT2 or HCF1 deregulated latency transcription and histone modifications at OriP, as well as the OriP-regulated latency type-dependent C promoter (Cp) and Q promoter (Qp). HCF1 depletion led to a loss of histone H3K4me3 (trimethylation of histone H3 at lysine 4) and H3 acetylation at Cp in type III latency and Qp in type I latency, as well as an increase in heterochromatic H3K9me3 at these sites. HCF1 depletion resulted in the loss of EBV episomes from Burkitt's lymphoma cells with type I latency and reactivation from lymphoblastoid cells (LCLs) with type III latency. These findings indicate that HCF1 and OCT2 function at OriP to regulate viral transcription, histone modifications, and episome maintenance. As HCF1 is best known for its function in herpes simplex virus 1 (HSV-1) immediate early gene transcription, our findings suggest that EBV latency transcription shares unexpected features with HSV gene regulation.IMPORTANCEEBV latency is associated with several human cancers. Viral latent cycle gene expression is regulated by the epigenetic control of the OriP enhancer region. Here, we show that cellular factors OCT2 and HCF1 bind OriP in association with EBNA1 to maintain elevated histone H3K4me3 and transcriptional enhancer function. HCF1 is known as a transcriptional coactivator of herpes simplex virus (HSV) immediate early (IE) transcription, suggesting that OriP enhancer shares aspects of HSV IE transcription control.

scholarly journals Control of Herpes Simplex Virus Replication Is Mediated through an Interferon Regulatory Factor 3-Dependent Pathway

2009 ◽  
Vol 83 (23) ◽  
pp. 12399-12406 ◽  
Author(s):  
Vineet D. Menachery ◽  
David A. Leib
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Replication ◽  
Early Recognition ◽  
Critical Role ◽  
Type I ◽  
Type I Ifn ◽  
Regulatory Factor ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT The type I interferon (IFN) cascade is critical in controlling viral replication and pathogenesis. Recognition pathways triggered by viral infection rapidly induce the type I IFN cascade, often in an IFN regulatory factor 3 (IRF-3)-dependent fashion. This dependence predicts that loss of IRF-3 would render early recognition pathways inoperative and thereby impact virus replication, but this has not been observed previously with herpes simplex virus type 1 (HSV-1) in vitro. In this study, HSV-1-infected IRF-3−/− bone marrow-derived dendritic cells (BMDCs) and macrophages supported increased HSV replication compared to control cells. In addition, IRF-3-deficient BMDCs exhibited delayed type I IFN synthesis compared to control cells. However, while IFN pretreatment of IRF-3−/− BMDCs resulted in reduced virus titers, a far greater reduction was seen after IFN treatment of wild-type cells. This suggests that even in the presence of exogenously supplied IFN, IRF-3−/− BMDCs are inherently defective in the control of HSV-1 replication. Together, these results demonstrate a critical role for IRF-3-mediated pathways in controlling HSV-1 replication in cells of the murine immune system.

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