scholarly journals 480. Alternate Diagnoses in Children Evaluated for Multisystem Inflammatory Syndrome in Children (MIS-C)

2021 ◽  
Vol 8 (Supplement_1) ◽  
pp. S341-S341
Author(s):  
Kelli Kaneta ◽  
Sindhu Mohandas ◽  
Jackie Szmuszkovicz ◽  
Sarah White ◽  
Susan Wu
Keyword(s):  
Urinary Tract Infection ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Rickettsial Infections ◽  
Exposure History ◽  
Epstein Barr ◽  
Simplex Virus ◽  
Inflammatory Syndrome ◽  
Prompt Diagnosis ◽  
Post Infectious

Abstract Background SARS-CoV-2 infection is typically a mild illness in children. Multisystem inflammatory syndrome in children (MIS-C) is a rare, post-infectious, hyperinflammatory condition associated with SARS-CoV-2 infection. The presentation of MIS-C is nonspecific and diagnostic criteria is broad. The Centers for Disease Control (CDC) defines MIS-C as a hospitalized patient < 21 years presenting with fever, laboratory evidence of inflammation, no alternative plausible diagnosis, and with positive exposure history or testing for current or recent SARS-CoV-2 infection. Since there is no single diagnostic test for MIS-C, there are other disease processes that can mimic its presentation and delay prompt diagnosis and management. Methods Between March 2020 and February 2021, we reviewed 282 charts of patients admitted for evaluation of MIS-C at our institution. Results 101 were found to have MIS-C, 45 found to have Kawasaki Disease (KD), and 129 were ruled out. Of the ruled-out group, the most common final diagnoses were viral infection, urinary tract infection, and acute SARS-CoV-2 infection. Other diagnoses included rickettsial infections, pneumonia, rheumatologic conditions, and bloodstream infection. Rhinovirus/enterovirus, adenovirus, Epstein-Barr virus (EBV), and Herpes Simplex Virus (HSV) were the most common viruses other than SARS-CoV-2 identified. Conclusion These findings highlight the importance of maintaining a broad differential when evaluating a patient for MIS-C, especially as community seroprevalence rises, making antibody presence less predictive of MIS-C. Disclosures Susan Wu, MD, Eli Lilly (Shareholder)

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 The Epstein-Barr Virus SM Protein Is Functionally Similar to ICP27 from Herpes Simplex Virus in Viral Infections

2002 ◽  
Vol 76 (18) ◽  
pp. 9420-9433 ◽  
Author(s):  
Julie L. Boyer ◽  
Sankar Swaminathan ◽  
Saul J. Silverstein
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Epstein Barr Virus ◽  
Common Mechanism ◽  
Barr Virus ◽  
Epstein Barr ◽  
Simplex Virus ◽  
Sm Protein ◽  
Hsv 1

ABSTRACT The herpes simplex virus type 1 (HSV-1) ICP27 protein is an essential RNA-binding protein that shuttles between the nucleus and cytoplasm to increase the cytoplasmic accumulation of viral late mRNAs. ICP27 homologs have been identified in each of the herpesvirus subfamilies, and accumulating evidence indicates that homologs from the gammaherpesvirus subfamily function similarly to ICP27. In particular, the Epstein-Barr virus (EBV) SM protein posttranscriptionally regulates gene expression, binds RNA in vitro and in vivo, and shuttles between the nucleus and cytoplasm. To determine if these two proteins function through a common mechanism, the ability of EBV SM to complement the growth defect of an HSV-1 ICP27-null virus was examined in a transient-expression assay. ICP27 stimulated the growth of the null mutant more efficiently than did SM, but the ability of SM to compensate for the ICP27 defects suggests conservation of common functions. To assay for complementation in the context of a viral infection, the growth properties of an HSV recombinant expressing SM in an ICP27-null background were analyzed. SM stimulated growth of the recombinant, although this growth was reduced by comparison to that of an ICP27-expressing virus. By contrast, an HSV recombinant expressing an SM mutant allele defective for transactivation activity and nucleocytoplasmic shuttling did not grow at all. These results suggest that SM and ICP27 may regulate gene expression through a common pathway that is evolutionarily conserved in herpesviruses.

scholarly journals Prevalence of Epstein-Barr virus, human papillomavirus, cytomegalovirus and herpes simplex virus type 1 in patients with diabetes mellitus type 2 in south-eastern Poland

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222607 ◽  
Author(s):  
Jakub Dworzański ◽  
Bartłomiej Drop ◽  
Ewa Kliszczewska ◽  
Małgorzata Strycharz-Dudziak ◽  
Małgorzata Polz-Dacewicz
Keyword(s):  
Diabetes Mellitus ◽  
Herpes Simplex ◽  
Diabetes Mellitus Type 2 ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Patients With Diabetes ◽  
Epstein Barr ◽  
Simplex Virus

Clinico-immunohistochemical aspects of recovery of reproductive function of women with chronic endometritis

2014 ◽  
Vol 63 (4) ◽  
pp. 34-38 ◽  
Author(s):  
Vera Aleksandrovna Kolmyk ◽  
Ruslan Abdullayevich Nasyrov ◽  
Galiya Fettyakhovna Kutusheva
Keyword(s):  
Epstein Barr Virus ◽  
Antiviral Drug ◽  
Progesterone Receptors ◽  
Reproductive Function ◽  
Clinical Analysis ◽  
Estrogen And Progesterone Receptors ◽  
Chronic Endometritis ◽  
Barr Virus ◽  
Epstein Barr ◽  
Simplex Virus

20 female patients aged 18-40 years old with a complicated anamnesis have been examined. Besides the regular clinical analysis the Pipel-byopsy was carried out with the immunohistochemical and histological investigation of the material. The expression level of estrogen and progesterone receptors has been determined. As well as the antigens of HSV, CMV and Epstein-Barr virus. In the case when chronic endometritis was diagnosed with the appearance of any of the viruses, the immunomodulating and antiviral therapy was administered. In the treatment of chronic endometritis associated with herpes simplex virus is advisable to administer an antiviral drug cour at least 3 months.

scholarly journals Epstein-Barr Virus mRNA Export Factor EB2 Is Essential for Production of Infectious Virus

2002 ◽  
Vol 76 (19) ◽  
pp. 9635-9644 ◽  
Author(s):  
Henri Gruffat ◽  
Julien Batisse ◽  
Dagmar Pich ◽  
Bernhard Neuhierl ◽  
Evelyne Manet ◽  
...  
Keyword(s):  
Dna Replication ◽  
Nuclear Export ◽  
Epstein Barr Virus ◽  
Alternative Pathway ◽  
Virus Production ◽  
Gene Encoding ◽  
Barr Virus ◽  
Cytoplasmic Accumulation ◽  
Epstein Barr ◽  
Simplex Virus

ABSTRACT The splicing machinery which positions a protein export complex near the exon-exon junction mediates nuclear export of mRNAs generated from intron-containing genes. Many Epstein-Barr virus (EBV) early and late genes are intronless, and an alternative pathway, independent of splicing, must export the corresponding mRNAs. Since the EBV EB2 protein induces the cytoplasmic accumulation of intronless mRNA, it is tempting to speculate that EB2 is a viral adapter involved in the export of intronless viral mRNA. If this is true, then the EB2 protein is essential for the production of EBV infectious virions. To test this hypothesis, we generated an EBV mutant in which the BMLF1 gene, encoding the EB2 protein, has been deleted (EBVBMLF1-KO). Our studies show that EB2 is necessary for the production of infectious EBV and that its function cannot be transcomplemented by a cellular factor. In the EBVBMLF1-KO 293 cells, oriLyt-dependent DNA replication was greatly enhanced by EB2. Accordingly, EB2 induced the cytoplasmic accumulation of a subset of EBV early mRNAs coding for essential proteins implicated in EBV DNA replication during the productive cycle. Two herpesvirus homologs of the EB2 protein, the herpes simplex virus type 1 protein ICP27 and, the human cytomegalovirus protein UL69, only partly rescued the phenotype of the EBVBMLF1-KO mutant, indicating that some EB2 functions in virus production cannot be transcomplemented by ICP27 and UL69.

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