scholarly journals Dynamics of Viral and Host Immune Cell MicroRNA Expression during Acute Infectious Mononucleosis

2018 ◽  
Vol 8 ◽  
Author(s):  
Vandana Kaul ◽  
Kenneth I. Weinberg ◽  
Scott D. Boyd ◽  
Daniel Bernstein ◽  
Carlos O. Esquivel ◽  
...  
2020 ◽  
Vol 32 (1) ◽  
Author(s):  
Raai Mahmood ◽  
Khalid Mohamed ◽  
Naba Saeed ◽  
Kadhim Al-Banaa ◽  
Jonathan Zimmerman ◽  
...  

Abstract Background Serum IgM (immunoglobulin M) testing is commonly used to diagnose acute viral infections. However, most clinicians are unaware of the vagaries of IgM testing, including antigenic cross-reactivity between multiple viruses and risk misdiagnosis. Case presentation We report a case of infectious mononucleosis with concomitantly positive IgM for EBV, CMV, VZV, and HSV. A 26-year-old man presented with acute infectious mononucleosis picture. His blood work showed a total bilirubin level of 7.7 mg/dl, ALT 1077 U/L, AST 806 U/L, ALP 325 U/L, and INR 1.0. Monospot was positive; peripheral blood smear showed atypical lymphocytes; however, because EBV infectious mononucleosis does not typically cause elevation of liver enzymes over 1000, other etiologies were explored. Tests for hepatitis A, B, C, HIV, ANA, and ASMA returned negative. IgM for EBV-VCA, CMV, HSV, and VZV all returned positive, and the diagnosis of EBV IM was called into question. Subsequent tests of CMV and HSV PCR for viral load were negative (VZV was not clinically suspected), and later on, EBV-EBNA returned negative and EBV-VCA IgM and IgG returned positive, confirming the diagnosis of acute EBV infection. Conclusion We believe that IgM seropositivity can result from cross-reactivity among several viruses (especially herpes viruses), and although often relied on, a positive IgM should not serve as the sole determinant for diagnosis of acute viral infections.


1990 ◽  
Vol 93 (5) ◽  
pp. 698-702 ◽  
Author(s):  
Susan L. Abbondanzo ◽  
Noriko Sato ◽  
Stephen E. Straus ◽  
Elaine S. Jaffe

2000 ◽  
Vol 109 (7) ◽  
pp. 531-537 ◽  
Author(s):  
Dedra S Buchwald ◽  
Tom D Rea ◽  
Wayne J Katon ◽  
Joan E Russo ◽  
Rhoda L Ashley

2004 ◽  
Vol 31 (2) ◽  
pp. 160-164 ◽  
Author(s):  
A.V. Atrasheuskaya ◽  
S.N. Kameneva ◽  
A.A. Neverov ◽  
G.M. Ignatyev

2021 ◽  
Vol 19 (1) ◽  
pp. 58-63
Author(s):  
J.-C. Khakizimana ◽  
◽  
V.N. Timchenko ◽  
V.P. Novikova ◽  
O.P. Gurina ◽  
...  

Objective. To analyze clinical and laboratory parameters, as well as the dynamics of cytokine production in children of different ages with acute infectious mononucleosis caused by Epstein-Barr virus (EBV mononucleosis). Patients and methods. We examined two groups of patients: group I included 20 children aged 1 to 7 years, whereas group II included 29 children aged 8 to 17 years. All study participants were tested in the acute phase of the disease and in early convalescence. We evaluated serum levels of interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and interferon-α (IFN-α) using enzyme-linked immunosorbent assay (ELISA) (standard Vektor-Best kits, Russia). Data analysis was performed using Microsoft Excel 2019 for Windows and IBM SPSS statistics; we applied the methods of non-parametric statistics. Differences were considered significant at p < 0.05. Results. The majority of children had fever, intoxication, acute tonsillitis, and enlarged cervical lymph nodes. Laboratory makers, such as lymphocytosis, neutropenia, and thrombocytopenia were more pronounced in children from group II. In both groups, the level of cytokines in the acute period of the disease was higher than the discriminatory one. In early convalescence, patients from group I demonstrated more significant reduction in the cytokine level than patients from group II (р < 0.05). In children over 7 years of age, the levels of IL-10 and TNF-α positively correlated with the disease duration (p < 0.01 and p < 0.05, respectively) Conclusion. The level of cytokine production in acute EBV mononucleosis depends on patients’ age. Concentrations of IL-10 and TNF-α can serve as markers reflecting the severity of EBV mononucleosis and can be used for disease prognosis. Key words: EBV mononucleosis, children, cytokines, IL-6, IL-10, TNF-α, IFN-α


1990 ◽  
Vol 6 (5) ◽  
pp. 323-329 ◽  
Author(s):  
Michael W. Stanley ◽  
Theresa A. Steeper ◽  
Charles A. Horwitz ◽  
Linda G. Burton ◽  
John G. Strickler ◽  
...  

2020 ◽  
Author(s):  
Jordann E. Trainor ◽  
KR Pooja ◽  
Nathan T. Mortimer

AbstractThe interactions between Drosophila melanogaster and the parasitoid wasps that infect Drosophila species provide an important model for understanding host-parasite relationships. Following parasitoid infection, D. melanogaster larvae mount a response in which immune cells (hemocytes) form a capsule around the wasp egg, which then melanizes leading to death of the parasitoid. Previous studies have found that host hemocyte load, the number of hemocytes available for the encapsulation response, and the production of lamellocytes, an infection induced hemocyte type, are major determinants of host resistance. Parasitoids have evolved various virulence mechanisms to overcome the immune response of the D. melanogaster host, including both active immune suppression by venom proteins and passive immune evasive mechanisms. We find that a previously undescribed parasitoid species, Asobara sp. AsDen, utilizes an active virulence mechanism to infect D. melanogaster hosts. Asobara sp. AsDen infection inhibits host hemocyte expression of msn, a member of the JNK signaling pathway, which plays a role in lamellocyte production. Asobara sp. AsDen infection restricts the production of lamellocytes as assayed by hemocyte cell morphology and altered msn expression. Our findings suggest that Asobara sp. AsDen venom targets host signaling to suppress immunity.DeclarationsFundingThis work was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number R35GM133760.Availability of data and materialSequence data has been deposited in GenBank under accession # MT498809. Custom BLAST databases are available on request to corresponding author.Authors’ contributionsConceived of or designed study: J.E.T., N.T.M.; Performed research: J.E.T., P.K.; Analyzed data: J.E.T., P.K., N.T.M.; Wrote the paper: J.E.T., P.K., N.T.M.


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