Herpes-simplex-Keratitis. Ein kurzer Überblick zur aktuellen Therapie

Behrens–Baumann, W.

doi:10.1055/s-0029-1245289

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…Other reviewers have also reasoned that antiviral agents are effective for HSV epithelial keratitis (Barker 2008; Behrens-Baumann 2010; Wei 2008) and recommended that interferon and débridement need further study. The finding that drug-related adverse effects on the ocular surface such as toxic punctate epithelial erosions were infrequent and not serious was corroborated by ophthalmic studies in antiviral pharmacovigilance (Chen 1989; Falcon 1981; Naito 1987).…”

Section: Discussionmentioning

confidence: 99%

Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis

Wilhelmus

2010

Cochrane Database of Systematic Reviews

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Section: Discussionmentioning

confidence: 99%

Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis

Wilhelmus

2010

Cochrane Database of Systematic Reviews

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“…While many cytokines showed elevated expression during infection with HSV-1 we focused on those which were elevated in the IRF-7 −/− and DKO populations, compared to control and IRF-3 −/− mice. Disruption of interferon signaling can inhibit the IFNγ negative feedback loop, leading to increased expression of the pro-inflammatory cytokine IFNγ (Ben-Asouli et al, 2002; Kaempfer, 2006). In agreement with this, IFNγ was only detectable in IRF-7 −/− and DKO mice, and expression of MIG (Farber, 1997), a biomarker for IFNγ activity was also higher in IRF-7 −/− and DKO mice (Fig 5A).…”

Section: Resultsmentioning

confidence: 99%

Synergistic control of herpes simplex virus pathogenesis by IRF-3, and IRF-7 revealed through non-invasive bioluminescence imaging

et al. 2013

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Interferon regulatory factors IRF-3 and IRF-7 are central to the establishment of the innate antiviral response. This study examines HSV-1 pathogenesis in IRF-3−/−, IRF-7−/− and double-deleted IRF3/7−/− (DKO) mice. Bioluminescence imaging of infection revealed that DKO mice developed visceral infection following corneal inoculation, along with increased viral burdens in all tissues relative to single knockout mice. While all DKO mice synchronously reached endpoint criteria 5 days post infection, the IRF-7−/− mice survived longer, indicating that although IRF-7 is dominant, IRF-3 also plays a role in controlling disease. Higher levels of systemic proinflammatory cytokines were found in IRF7−/− and DKO mice relative to wild-type and IRF-3−/− mice, and IL-6 and G-CSF, indicative of sepsis, were increased in the DKO mice relative to wild-type or single-knockout mice. In addition to controlling viral replication, IRF-3 and −7 therefore play coordinating roles in modulation of inflammation during HSV infection.

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“…During HSV-1 infection, the virus preferentially invades cranial nerves where it is able to establish latency in neurons in cranial ganglia, which can persist for the lifetime of the host [Whitley et al, 1998;Liu et al, 2015]. HSV-1 infection most commonly manifests as orofacial lesions, including hepatitis, meningitis, encephalitis, and stromal keratitis [Baringer 2008;Behrens-Baumann 2010;Murphy et al, 2013].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐649 promotes HSV‐1 replication by directly targeting MALT1

Zhang

Dai

Tang

et al. 2016

Journal of Medical Virology

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Herpes simplex virus type 1 (HSV-1), a member of the Herpes viridae, is associated with a wide variety of nervous system diseases including meningitis and encephalitis. The data presented here demonstrate that miR-649 promotes the replication of HSV-1 without affecting cell viability. Further mechanistic studies revealed that MALT1 (mucosa associated lymphoid tissue lymphoma translocation gene 1) is directly targeted by miR-649. We then found that MALT1 and the downstream NF-κB signaling pathway, are involved in miR-649-induced HSV-1 replication. Interestingly, miR-649 levels were downregulated after HSV-1 infection, and miR-649 expression was negatively associated with MALT1 expression in HSV-1-infected HeLa cells. Taken together, this present study indicates that miR-649 promotes HSV-1 replication through regulation of the MALT1-mediated antiviral signaling pathway and suggests a promising target for antiviral therapies. J. Med. Virol. 89:1069-1079, 2017. © 2016 Wiley Periodicals, Inc.

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Herpes-simplex-Keratitis. Ein kurzer Überblick zur aktuellen Therapie

Cited by 9 publications

References 37 publications

Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis

Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis

Synergistic control of herpes simplex virus pathogenesis by IRF-3, and IRF-7 revealed through non-invasive bioluminescence imaging

MicroRNA‐649 promotes HSV‐1 replication by directly targeting MALT1

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