Towards an in vitro model for acute hemorrhagic conjunctivitis: cytokine-mediated vascular endothelial cell activation triggered by enterovirus type 70 infection

Chang, Cheng-Hsien; Lin, Kuei-Hsiang; Anderson, Robert

doi:10.1016/j.jcv.2003.07.003

Cited by 4 publications

(4 citation statements)

References 35 publications

(31 reference statements)

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“…Endothelial cell activation could not be detected after EV‐94 infection (data not shown), even though activation promoting cytokines, for example, IL‐1A, which has been shown to be the predominant endothelial cell activating factor after EV‐70 infection [Chang et al, 2004], were detected. This may be due to the rapid lysis of endothelial cells following high m.o.i.…”

Section: Discussionmentioning

confidence: 94%

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Cellular tropism of human enterovirus D species serotypes EV‐94, EV‐70, and EV‐68 in vitro: Implications for pathogenesis

Smura¹,

Ylipaasto²,

Klemola³

et al. 2010

Journal of Medical Virology

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Enterovirus 94 (EV‐94) is an enterovirus serotype described recently which, together with EV‐68 and EV‐70, forms human enterovirus D species. This study investigates the seroprevalences of these three serotypes and their abilities to infect, replicate, and damage cell types considered to be essential for enterovirus‐induced diseases. The cell types studied included human leukocyte cell lines, primary endothelial cells, and pancreatic islets. High prevalence of neutralizing antibodies against EV‐68 and EV‐94 was found in the Finnish population. The virus strains studied had wide leukocyte tropism. EV‐94 and EV‐68 were able to produce infectious progeny in leukocyte cell lines with monocytic, granulocytic, T‐cell, or B‐cell characteristics. EV‐94 and EV‐70 were capable of infecting primary human umbilical vein endothelial cells, whereas EV‐68 had only marginal progeny production and did not induce cytopathic effects in these cells. Intriguingly, EV‐94 was able to damage pancreatic islet β‐cells, to infect, replicate, and cause necrosis in human pancreatic islets, and to induce proinflammatory and chemoattractive cytokine expression in endothelial cells. These results suggest that HEV‐D viruses may be more prevalent than has been thought previously, and they provide in vitro evidence that EV‐94 may be a potent pathogen and should be considered a potentially diabetogenic enterovirus type. J. Med. Virol. 82:1940–1949, 2010. © 2010 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 94%

“…EV‐94 infection. Some other enterovirus serotypes (e.g., CBV‐2, CBV‐4, CBV‐5, CVA‐9, CVA‐13, E‐1, E‐11, E‐30, PV‐1, EV‐70, and EV‐71) have been shown to induce endothelial cell activation [Saijets et al, 2003; Chang et al, 2004; Liang et al, 2004; Zanone et al, 2007].…”

Section: Discussionmentioning

confidence: 99%

Cellular tropism of human enterovirus D species serotypes EV‐94, EV‐70, and EV‐68 in vitro: Implications for pathogenesis

Smura¹,

Ylipaasto²,

Klemola³

et al. 2010

Journal of Medical Virology

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“…The pathophysiological mechanisms of virus-induced conjunctival inflammation may include direct virus-mediated effects during replication in conjunctival epithelium or vascular endothelium, humoral and cellular immune-mediated mechanisms, and secondary infection resultant from virus-induced structural or functional alterations in the conjunctiva. 18,19 The objectives of the study reported here were to determine the frequency of viral detection in conjunctival samples from client-owned dogs with naturally acquired idiopathic conjunctivitis and to identify signalment, historical, and clinical findings that are positively correlated with viral detection. In addition to relatively nonspecific isolation methods of viral detection, molecular assays for specific viruses were used.…”

mentioning

confidence: 99%

Virologic survey of dogs with naturally acquired idiopathic conjunctivitis

Ledbetter

Hornbuckle²,

Dubovi³

2009

javma

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“… 1 , 6 , 10 The conjunctivitis is caused by virus-induced effects on conjunctival, corneal, and vascular endothelial cells. 8 , 22 Ocular host defenses against EV70 and CA24v infection include profuse tearing and conjunctival inflammation with local production of interferon (IFN) and virus-specific neutralizing activity. 23 – 26 These ocular host defenses likely act together to rapidly clear the IFN-sensitive enteroviruses and limit ocular symptoms 27 – 29 but do not prevent secondary CA24v infection of the upper respiratory tract 7 or EV70 neuropathy observed more commonly in males.…”

Section: Introductionmentioning

confidence: 99%

Acute hemorrhagic conjunctivitis: anti-coxsackievirus A24 variant secretory immunoglobulin A in acute and convalescent tear

Langford¹,

Anders²,

Burch³

2015

OPTH

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PurposeThe purpose of this paper is to present the clinical course of a laboratory-acquired case of acute hemorrhagic conjunctivitis (AHC) caused by coxsackievirus A24 variant (CA24v). Also, the anti-CA24v neutralizing activity and anti-CA24v immunoglobulin (Ig) G and secretory IgA (sIgA) in acute and convalescent tears and/or sera are presented.CaseA 60-year-old male presented with acute-onset left eyelid edema, tearing, conjunctival erythema, pain, foreign body sensation, and subconjunctival hemorrhage 24 hours after suspected laboratory exposure. Bilateral conjunctivitis presented 24 hours later and resolved in 10 days.MethodsTear and blood samples were collected for virus isolation and neutralizing assays. CA24v-reactive IgG and sIgA in tear and/or serum samples were detected by immunofluorescent antibody analysis of ethanol-fixed virus-infected cells.ResultsPeak tear neutralization titers (1,000–1,500 U/mL) against the isolated virus occurred 1 day post-onset (po) of AHC. Tear neutralization titers became undetectable by the sixth day as serum neutralization titers became detectable on the ninth day po (60 U/mL), peaked by 21 days (3,000 U/mL), declined by 1 year to 200 U/mL, and remained at 30 U/mL 5 years po. Antibody to human IgG, IgA, and secretory component (sIgA) reacted with CA24v-infected cells treated with pooled acute tears collected 1–4 days po. Predominantly, sIgA was detected in CA24v-infected cells treated with tears collected 4 years and 5 years post-AHC, while convalescent serum contained predominantly anti-CA24v IgG.ConclusionAHC was confirmed by CA24v isolation, tear anti-CA24v neutralizing activity, and seroconversion. The detection of CA24v-reactive IgG, sIgA, and neutralizing activity in tears collected 1–4 days po of AHC supports plasma extravasation of IgG and suggests a defensive role for tear anti-CA24v sIgA. The results suggest that immunofluorescent antibody analysis of tears for persistent anti-CA24v sIgA may be useful in epidemiological monitoring of AHC.

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Towards an in vitro model for acute hemorrhagic conjunctivitis: cytokine-mediated vascular endothelial cell activation triggered by enterovirus type 70 infection

Cited by 4 publications

References 35 publications

Cellular tropism of human enterovirus D species serotypes EV‐94, EV‐70, and EV‐68 in vitro: Implications for pathogenesis

Cellular tropism of human enterovirus D species serotypes EV‐94, EV‐70, and EV‐68 in vitro: Implications for pathogenesis

Virologic survey of dogs with naturally acquired idiopathic conjunctivitis

Acute hemorrhagic conjunctivitis: anti-coxsackievirus A24 variant secretory immunoglobulin A in acute and convalescent tear

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