Severe Hepatitis Associated with an Echovirus 18 Infection in an Immune-Compromised Adult

Lefterova, Martina I.; Rivetta, Claudia V.; George, Tracy I.; Pinsky, Benjamin A.

doi:10.1128/jcm.02405-12

Cited by 15 publications

(15 citation statements)

References 14 publications

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“…However, immunodeficient individuals, including adults, are more susceptible to echovirus infections, which often induces hepatitis [33][34][35][36] . In addition, analysis of mutations in the E11 genome induced by selective pressure in an immunodeficient individual who developed chronic infection revealed strikingly high sequence conservation in the 3C virally-encoded protease which often attenuates host cell innate immune signaling 36 .…”

Section: Discussionmentioning

confidence: 99%

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Wells

Grimes

Kim

et al. 2020

Preprint

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Neonatal echovirus infections are characterized by severe hepatitis and neurological complications that can be fatal. Here, we show that expression of the human homologue of the neonatal Fc receptor (hFcRn), the primary receptor for echoviruses, and ablation of type I interferon (IFN) signaling are key host determinants involved in echovirus pathogenesis. We show that expression of hFcRn alone is insufficient to confer susceptibility to echovirus infections in mice. However, expression of hFcRn in mice deficient in type I interferon (IFN) signaling, hFcRn-IFNAR−/−, recapitulate the echovirus pathogenesis observed in humans. Luminex-based multianalyte profiling from E11 infected hFcRn-IFNAR−/− mice revealed a robust systemic immune response to infection, including the induction of type I IFNs. Furthermore, similar to the severe hepatitis observed in humans, E11 infection in hFcRn-IFNAR−/− mice caused profound liver damage. Our findings define the host factors involved in echovirus pathogenesis and establish in vivo models that recapitulate echovirus disease.

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Section: Discussionmentioning

confidence: 99%

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Wells

Grimes

Kim

et al. 2020

Preprint

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“…Headache, low-grade fever, nuchal rigidity and vomiting were the most prominent symptoms while rash or diarrhoea occurred in 5-6 % of patients [13]. Noteworthily, also severe and disseminated courses with a sepsis-like picture have been observed particularly in immunocompromised patients and neonates [14][15][16]. Recently, a case of fatal E-18 encephalitis in an 18-month-old infant was reported [17].…”

Section: Introductionmentioning

confidence: 93%

Analysis of an echovirus 18 outbreak in Thuringia, Germany: insights into the molecular epidemiology and evolution of several enterovirus species B members

Krumbholz

Egerer

Braun

et al. 2016

Med Microbiol Immunol

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In October and November 2010, six children and one woman were presented with symptoms of aseptic meningitis in Jena, Thuringia, Germany. Enterovirus RNA was detected in the cerebrospinal fluid of all patients by RT-PCR, and preliminary molecular typing revealed echovirus 18 (E-18) as causative agent. Virus isolates were obtained from stool samples of three patients and several contact persons. Again, most isolates were typed as E-18. In addition, coxsackievirus B5 (CV-B5) and echovirus 25 (E-25) were found to co-circulate. As only few complete E-18 sequences are available in GenBank, the entire genomes of these isolates were determined using direct RNA-sequencing technology. We did not find evidence for recombination between E-18, E-25 or CV-B5 during the outbreak. Viral protein 1 gene sequences and the cognate 3D polymerase gene sequences of each isolate and GenBank sequences were analysed in order to define type-specific recombination groups (recogroups).

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“…In temperate regions, infections are most common in summer and fall, whereas in tropical regions infections occur throughout the year. Age has a strong association with clinical presentation: central nervous system (CNS) disease occurs most frequently in [5][6][7][8][9][10][11][12][13][14][15] year-olds, myocarditis in 20-40 year-olds, severe infections (including myocarditis, CNS disease and sepsis-like illness) in neonates and infants, and hand, foot and mouth disease in children aged < 5 years. A risk factor for infection is low socioeconomic status, most likely associated with poor sanitation and close living quarters.…”

Section: Introductionmentioning

confidence: 99%

Tissue tropism, pathology and pathogenesis of enterovirus infection

Muehlenbachs

Bhatnagar

Zaki

2014

The Journal of Pathology

147

121

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Enteroviruses are very common and cause infections with a diverse array of clinical features. Enteroviruses are most frequently considered by practising pathologists in cases of aseptic meningitis, encephalitis, myocarditis and disseminated infections in neonates and infants. Congenital infections have been reported and transplacental transmission is thought to occur. Although skin biopsies during hand, foot and mouth disease are infrequently obtained, characteristic dermatopathological findings can be seen. Enteroviruses have been implicated in lower respiratory tract infections. This review highlights histopathological features of enterovirus infection and discusses diagnostic modalities for formalin-fixed paraffin-embedded tissues and their associated pitfalls. Immunohistochemistry can detect enterovirus antigen within cells of affected tissues; however, assays can be non-specific and detect other viruses. Molecular methods are increasingly relied upon but, due to the high frequency of asymptomatic enteroviral infections, clinical-pathological correlation is needed to determine significance. Of note, diagnostic assays on central nervous system or cardiac tissues from immunocompetent patients with prolonged disease courses are most often negative. Histopathological, immunohistochemical and molecular studies performed on clinical specimens also provide insight into enteroviral tissue tropism and pathogenesis.

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Severe Hepatitis Associated with an Echovirus 18 Infection in an Immune-Compromised Adult

Cited by 15 publications

References 14 publications

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Human FcRn expression and Type I Interferon signaling control Echovirus 11 pathogenesis in mice

Analysis of an echovirus 18 outbreak in Thuringia, Germany: insights into the molecular epidemiology and evolution of several enterovirus species B members

Tissue tropism, pathology and pathogenesis of enterovirus infection

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