Authors:
Elena Nikolaevna Filatova Laboratory of Molecular Biology and Biotechnology, Blokhina Scientific Research Institute of Epidemiology and Microbiology of Nizhny Novgorod, Nizhny Novgorod, Russian Federation

Search for other papers by Elena Nikolaevna Filatova in
Current site
Google Scholar
PubMed
Close
,
Nikolay Aleksandrovich Sakharnov Laboratory of Molecular Biology and Biotechnology, Blokhina Scientific Research Institute of Epidemiology and Microbiology of Nizhny Novgorod, Nizhny Novgorod, Russian Federation

Search for other papers by Nikolay Aleksandrovich Sakharnov in
Current site
Google Scholar
PubMed
Close
,
Dmitry Igorevich Knyazev Laboratory of Molecular Biology and Biotechnology, Blokhina Scientific Research Institute of Epidemiology and Microbiology of Nizhny Novgorod, Nizhny Novgorod, Russian Federation

Search for other papers by Dmitry Igorevich Knyazev in
Current site
Google Scholar
PubMed
Close
, and
Oleg Vladimirovich Utkin Laboratory of Molecular Biology and Biotechnology, Blokhina Scientific Research Institute of Epidemiology and Microbiology of Nizhny Novgorod, Nizhny Novgorod, Russian Federation

Search for other papers by Oleg Vladimirovich Utkin in
Current site
Google Scholar
PubMed
Close
Restricted access

Transforming growth factor β 1 (TGFB1) likely contributes to the pathogenesis of Epstein-Barr virus (EBV)-mediated cancer. A microarray containing 59 probes for detecting mRNA of members of TGFB1-associated pathways was developed. mRNA expression of TGFB1 receptors and members of connected pathways were examined in peripheral blood leukocytes of patients during acute EBV infection and after recovery. TGFB1 and TGFBR2 mRNA expression was increased in patients with EBV infection. Similarly, mRNA expression of protein kinase C (PRKCB), MAP3K7, PDLIM7, and other members of TGFB1 and NF-κB signaling pathways increased. A shift of mRNA transcript variant expression of some key members (TGFBR2, PRKCB, and NFKBIB) of involved signaling pathways was detected. After the patients’ recovery, most of the altered mRNA expression has been normalized. We speculate that in patients with EBV infection, members of TGFB1-associated pathways contribute to the suppression of proapoptotic and induction of pro-survival factors in leukocytes. The modulation of TGFB1-associated pathways may be considered as a potential risk factor in the development of EBV-associated tumors in patients with acute EBV infection.

Supplementary Materials

    • Supplementary Material
  • 1.

    Dojcinov, S. D. , Fend, F. , Quintanilla-Martinez, L. : EBV-positive lymphoproliferations of B- T- and NK-cell derivation in non-immunocompromised hosts. Pathogens 7, 28 (2018).

    • Search Google Scholar
    • Export Citation
  • 2.

    Yan, X. , Xiong, X. , Chen, Y.-G. : Feedback regulation of TGF-β signaling. Acta Biochim Biophys Sin 50, 3750 (2018).

  • 3.

    Iempridee, T. , Das, S. , Xu, I. , Mertz, J. E. : Transforming growth factor β-induced reactivation of Epstein-Barr virus involves multiple Smad-binding elements cooperatively activating expression of the latent-lytic switch BZLF1 gene. J Virol 85, 78367848 (2011).

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4.

    Xu, J. , Menezes, J. , Prasad, U. , Ahmad, A. : Elevated serum levels of transforming growth factor β1 in Epstein-Barr virus-associated nasopharyngeal carcinoma patients. Int J Cancer 84, 396399 (1999).

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5.

    Xie, L. , Law, B. K. , Chytil, A. M. , Brown, K. A. , Aakre, M. E. , Moses, H. L. : Activation of the Erk pathway is required for TGF-β1-induced EMT in vitro. Neoplasia (New York, NY) 6, 603610 (2004).

    • Search Google Scholar
    • Export Citation
  • 6.

    Fukuda, M. , Kurosaki, W. , Yanagihara, K. , Kuratsune, H. , Sairenji, T. : A mechanism in Epstein-Barr virus oncogenesis: Inhibition of transforming growth factor-β1-mediated induction of MAPK/p21 by LMP1. Virology 302, 310320 (2002).

    • Search Google Scholar
    • Export Citation
  • 7.

    Al-Azayzih, A. , Gao, F. , Goc, A. , Somanath, P. R. : TGF β1 induces apoptosis in invasive prostate cancer and bladder cancer cells via Akt-independent, p38 MAPK and JNK/SAPK-mediated activation of caspases. Biochem Biophys Res Commun 427, 165170 (2012).

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8.

    Bailey, K. L. , Agarwal, E. , Chowdhury, S. , Luo, J. , Brattain, M. G. , Black, J. D. , Wang, J. : TGFβ/Smad3 regulates proliferation and apoptosis through IRS-1 inhibition in colon cancer cells. PLoS One 12, e0176096 (2017).

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9.

    Freudlsperger, C. , Bian, Y. , Contag Wise, S. , Burnett, J. , Coupar, J. : TGF-β and NF-κB signal pathway cross-talk is mediated through TAK1 and SMAD7 in a subset of head and neck cancers. Oncogene 32, 15491559 (2013).

    • Search Google Scholar
    • Export Citation
  • 10.

    Yakymovych, I. , Ten Dijke, P. , Heldin, C.H. , Souchelnytskyi, S. : Regulation of Smad signaling by protein kinase C. FASEB J 15, 553555 (2001).

  • 11.

    Kawakami, T. , Kawakami, Y. , Kitaura, J. : Protein kinase C beta (PKC beta): Normal functions and diseases. J Biochem (Tokyo) 132, 677682 (2002).

    • Search Google Scholar
    • Export Citation
  • 12.

    Krappmann, D. , Patke, A. , Heissmeyer, V. , Scheidereit, C. : B-cell receptor- and phorbol ester-induced NF-κB and c-Jun N-terminal kinase activation in B cells requires novel protein kinase C’s. Mol Cell Biol 21, 66406650 (2001).

    • Search Google Scholar
    • Export Citation
  • 13.

    Uemura, N. , Kajino, T. , Sanjo, H. , Sato, S. , Akira, S. , Matsumoto, K. , Ninomiya-Tsuji, J. : Tak1 is a component of the Epstein-Barr virus Lmp1 complex and is essential for activation of JNK but not of NF-κB. J Biol Chem 281, 78637872 (2006).

    • Search Google Scholar
    • Export Citation
  • 14.

    Solntsev, L. A. , Starikova, V. D. , Sakharnov, N. A. , Knyazev, D. I. , Utkin, O. V. : Strategy of probe selection for studying mRNAs that participate in receptor-mediated apoptosis signaling. Mol Biol 49, 457465 (2015).

    • Search Google Scholar
    • Export Citation
  • 15.

    Wu, Z. , Aryee, M. J. : Subset quantile normalization using negative control features. J Comput Biol 17, 13851395 (2010).

  • 16.

    Wu, Y. , Su, M. , Zhang, S. , Cheng, Y. , Liao, X. Y. , Lin, B. Y. , Chen, Y. Z. : Abnormal expression of TGF-beta type II receptor isoforms contributes to acute myeloid leukemia. Oncotarget 8, 1003710049 (2016).

    • Search Google Scholar
    • Export Citation
  • 17.

    Wan, J. , Sun, L. , Mendoza, J. W. , Chui, Y. L. , Huang, D. P. : Elucidation of the c-Jun N-terminal kinase pathway mediated by Epstein-Barr virus-encoded latent membrane protein 1. Mol Cell Biol 24, 192199 (2004).

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 18.

    Dowling, C. M. , Phelan, J. , Callender, J. A. , Cathcart, M. C. , Mehigan, B. : Protein kinase C beta II suppresses colorectal cancer by regulating IGF-1 mediated cell survival. Oncotarget 7, 2091920933 (2016).

    • PubMed
    • Search Google Scholar
    • Export Citation
  • Collapse
  • Expand

Senior editors

Editor-in-Chief: Prof. Dóra Szabó (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)

Managing Editor: Dr. Béla Kocsis (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)

Co-editor: Dr. Andrea Horváth (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)

Editorial Board

  • Prof. Éva ÁDÁM (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Sebastian AMYES (Department of Medical Microbiology, University of Edinburgh, Edinburgh, UK.)
  • Dr. Katalin BURIÁN (Institute of Clinical Microbiology University of Szeged, Szeged, Hungary; Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary.)
  • Dr. Orsolya DOBAY (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Ildikó Rita DUNAY (Institute of Inflammation and Neurodegeneration, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany)
  • Prof. Levente EMŐDY(Department of Medical Microbiology and Immunology, University of Pécs, Pécs, Hungary.)
  • Prof. Anna ERDEI (Department of Immunology, Eötvös Loránd University, Budapest, Hungary, MTA-ELTE Immunology Research Group, Eötvös Loránd University, Budapest, Hungary.)
  • Prof. Éva Mária FENYŐ (Division of Medical Microbiology, University of Lund, Lund, Sweden)
  • Prof. László FODOR (Department of Microbiology and Infectious Diseases, University of Veterinary Medicine, Budapest, Hungary)
  • Prof. József KÓNYA (Department of Medical Microbiology, University of Debrecen, Debrecen, Hungary)
  • Prof. Yvette MÁNDI (Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary)
  • Prof. Károly MÁRIALIGETI (Department of Microbiology, Eötvös Loránd University, Budapest, Hungary)
  • Prof. János MINÁROVITS (Department of Oral Biology and Experimental Dental Research, University of Szeged, Szeged, Hungary)
  • Prof. Béla NAGY (Centre for Agricultural Research, Institute for Veterinary Medical Research, Budapest, Hungary.)
  • Prof. István NÁSZ (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Kristóf NÉKÁM (Hospital of the Hospitaller Brothers in Buda, Budapest, Hungary.)
  • Dr. Eszter OSTORHÁZI (Institute of Medical Microbiology, Semmelweis University, Budapest, Hungary)
  • Prof. Rozália PUSZTAI (Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary)
  • Prof. Peter L. RÁDY (Department of Dermatology, University of Texas, Houston, Texas, USA)
  • Prof. Éva RAJNAVÖLGYI (Department of Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary)
  • Prof. Ferenc ROZGONYI (Institute of Laboratory Medicine, Semmelweis University, Budapest, Hungary)
  • Prof. Joseph G. SINKOVICS (The Cancer Institute, St. Joseph’s Hospital, Tampa, Florida, USA)
  • Prof. Júlia SZEKERES (Department of Medical Biology, University of Pécs, Pécs, Hungary.)
  • Prof. Mária TAKÁCS (National Reference Laboratory for Viral Zoonoses, National Public Health Center, Budapest, Hungary.)
  • Prof. Edit URBÁN (Department of Medical Microbiology and Immunology University of Pécs, Pécs, Hungary; Institute of Translational Medicine, University of Pécs, Pécs, Hungary.)

 

Editorial Office:
Akadémiai Kiadó Zrt.
Budafoki út 187-187, A/3, H-1117 Budapest, Hungary

Editorial Correspondence:
Acta Microbiologica et Immunologica Hungarica
Institute of Medical Microbiology
Semmelweis University
P.O. Box 370
H-1445 Budapest, Hungary
Phone: + 36 1 459 1500 ext. 56101
Fax: (36 1) 210 2959
E-mail: amih@med.semmelweis-univ.hu

 Indexing and Abstracting Services:

  • Biological Abstracts
  • BIOSIS Previews
  • CAB Abstracts
  • CABELLS Journalytics
  • Chemical Abstracts
  • Global Health
  • Index Medicus
  • Index Veterinarius
  • Medline
  • Referativnyi Zhurnal
  • SCOPUS
  • Science Citation Index Expanded

2023  
Web of Science  
Journal Impact Factor 1.3
Rank by Impact Factor Q4 (Immunology)
Journal Citation Indicator 0.31
Scopus  
CiteScore 2.3
CiteScore rank Q3 (Infectious Diseases)
SNIP 0.389
Scimago  
SJR index 0.308
SJR Q rank Q3

Acta Microbiologica et Immunologica Hungarica
Publication Model Hybrid
Submission Fee none
Article Processing Charge 1100 EUR/article (only for OA publications)
Regional discounts on country of the funding agency World Bank Lower-middle-income economies: 50%
World Bank Low-income economies: 100%
Further Discounts Editorial Board / Advisory Board members: 50%
Corresponding authors, affiliated to an EISZ member institution subscribing to the journal package of Akadémiai Kiadó: 100%
Subscription fee 2025 Online subsscription: 772 EUR / 848 USD
Print + online subscription: 860 EUR / 944 USD
Subscription Information Online subscribers are entitled access to all back issues published by Akadémiai Kiadó for each title for the duration of the subscription, as well as Online First content for the subscribed content.
Purchase per Title Individual articles are sold on the displayed price.

Acta Microbiologica et Immunologica Hungarica
Language English
Size A4
Year of
Foundation
1954
Volumes
per Year
1
Issues
per Year
4
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 1217-8950 (Print)
ISSN 1588-2640 (Online)

Monthly Content Usage

Abstract Views Full Text Views PDF Downloads
Apr 2024 42 0 0
May 2024 36 0 0
Jun 2024 15 0 1
Jul 2024 43 0 0
Aug 2024 27 0 0
Sep 2024 45 0 0
Oct 2024 19 1 1