A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections

Keiji Iwatsuki, Takenobu Yamamoto, Kazuhide Tsuji, Daisuke Suzuki, Kazuyasu Fujii, Hironori Matsuura, Takashi Oono

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Epstein-Barr virus (EBV), or human herpesvirus 4 (HHV-4), infects the vast majority of adults worldwide, and establishes both nonproductive (latent) and productive (lytic) infections. Host immune responses directed against both the lytic and latent cycle-associated EBV antigens induce a diversity of clinical symptoms in patients with chronic active EBV infections who usually contain an oligoclonal pool of EBV-infected lymphocyte subsets in their blood. Episomal EBV genes in the latent infection utilize an array of evasion strategies from host immune responses: the minimized expression of EBV antigens targeted by host cytotoxic T lymphocytes (CTLs), the down-regulation of cell adhesion molecule expression, and the release of virokines to inhibit the host CTLs. The oncogenic role of latent EBV infection is not yet fully understood, but latent membrane proteins (LMPs) expressed during the latency cycle have essential biological properties leading to cellular gene expression and immortalization, and EBV-encoded gene products such as viral interleukin-10 (vIL-10) and bcl-2 homologue function to survive the EBV-infected cells. The subsequent oncogenic DNA damage may lead to the development of neoplasms. EBV-associated NK/T cell lymphoproliferative disorders are prevalent in Asia, but quite rare in Western countries. The genetic immunological background, therefore, is closely linked to the development of EBV-associated neoplasms.

Original languageEnglish
Pages (from-to)169-180
Number of pages12
JournalActa Medica Okayama
Volume58
Issue number4
Publication statusPublished - Aug 2004

Fingerprint

Epstein-Barr Virus Infections
Human Herpesvirus 4
Viruses
T-cells
Cytotoxic T-Lymphocytes
Genes
Satellite Viruses
Antigens
Lymphoproliferative Disorders
Lymphocyte Subsets
Cell Adhesion Molecules
Lymphocytes
Infection
Natural Killer Cells
Interleukin-10
DNA Damage
Gene expression
Neoplasms
Membrane Proteins
Down-Regulation

Keywords

  • Chronic active EB virus infection
  • Hemophagocytic syndrome
  • Hydroa vacciniforme
  • Latent infection
  • Mosquito allergy

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Iwatsuki, K., Yamamoto, T., Tsuji, K., Suzuki, D., Fujii, K., Matsuura, H., & Oono, T. (2004). A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections. Acta Medica Okayama, 58(4), 169-180.

A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections. / Iwatsuki, Keiji; Yamamoto, Takenobu; Tsuji, Kazuhide; Suzuki, Daisuke; Fujii, Kazuyasu; Matsuura, Hironori; Oono, Takashi.

In: Acta Medica Okayama, Vol. 58, No. 4, 08.2004, p. 169-180.

Research output: Contribution to journalArticle

Iwatsuki, K, Yamamoto, T, Tsuji, K, Suzuki, D, Fujii, K, Matsuura, H & Oono, T 2004, 'A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections', Acta Medica Okayama, vol. 58, no. 4, pp. 169-180.
Iwatsuki K, Yamamoto T, Tsuji K, Suzuki D, Fujii K, Matsuura H et al. A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections. Acta Medica Okayama. 2004 Aug;58(4):169-180.
Iwatsuki, Keiji ; Yamamoto, Takenobu ; Tsuji, Kazuhide ; Suzuki, Daisuke ; Fujii, Kazuyasu ; Matsuura, Hironori ; Oono, Takashi. / A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections. In: Acta Medica Okayama. 2004 ; Vol. 58, No. 4. pp. 169-180.
@article{3222054c87d14ebfa5936bb8478a2e75,
title = "A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections",
abstract = "Epstein-Barr virus (EBV), or human herpesvirus 4 (HHV-4), infects the vast majority of adults worldwide, and establishes both nonproductive (latent) and productive (lytic) infections. Host immune responses directed against both the lytic and latent cycle-associated EBV antigens induce a diversity of clinical symptoms in patients with chronic active EBV infections who usually contain an oligoclonal pool of EBV-infected lymphocyte subsets in their blood. Episomal EBV genes in the latent infection utilize an array of evasion strategies from host immune responses: the minimized expression of EBV antigens targeted by host cytotoxic T lymphocytes (CTLs), the down-regulation of cell adhesion molecule expression, and the release of virokines to inhibit the host CTLs. The oncogenic role of latent EBV infection is not yet fully understood, but latent membrane proteins (LMPs) expressed during the latency cycle have essential biological properties leading to cellular gene expression and immortalization, and EBV-encoded gene products such as viral interleukin-10 (vIL-10) and bcl-2 homologue function to survive the EBV-infected cells. The subsequent oncogenic DNA damage may lead to the development of neoplasms. EBV-associated NK/T cell lymphoproliferative disorders are prevalent in Asia, but quite rare in Western countries. The genetic immunological background, therefore, is closely linked to the development of EBV-associated neoplasms.",
keywords = "Chronic active EB virus infection, Hemophagocytic syndrome, Hydroa vacciniforme, Latent infection, Mosquito allergy",
author = "Keiji Iwatsuki and Takenobu Yamamoto and Kazuhide Tsuji and Daisuke Suzuki and Kazuyasu Fujii and Hironori Matsuura and Takashi Oono",
year = "2004",
month = "8",
language = "English",
volume = "58",
pages = "169--180",
journal = "Acta Medica Okayama",
issn = "0386-300X",
publisher = "Okayama University",
number = "4",

}

TY - JOUR

T1 - A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections

AU - Iwatsuki, Keiji

AU - Yamamoto, Takenobu

AU - Tsuji, Kazuhide

AU - Suzuki, Daisuke

AU - Fujii, Kazuyasu

AU - Matsuura, Hironori

AU - Oono, Takashi

PY - 2004/8

Y1 - 2004/8

N2 - Epstein-Barr virus (EBV), or human herpesvirus 4 (HHV-4), infects the vast majority of adults worldwide, and establishes both nonproductive (latent) and productive (lytic) infections. Host immune responses directed against both the lytic and latent cycle-associated EBV antigens induce a diversity of clinical symptoms in patients with chronic active EBV infections who usually contain an oligoclonal pool of EBV-infected lymphocyte subsets in their blood. Episomal EBV genes in the latent infection utilize an array of evasion strategies from host immune responses: the minimized expression of EBV antigens targeted by host cytotoxic T lymphocytes (CTLs), the down-regulation of cell adhesion molecule expression, and the release of virokines to inhibit the host CTLs. The oncogenic role of latent EBV infection is not yet fully understood, but latent membrane proteins (LMPs) expressed during the latency cycle have essential biological properties leading to cellular gene expression and immortalization, and EBV-encoded gene products such as viral interleukin-10 (vIL-10) and bcl-2 homologue function to survive the EBV-infected cells. The subsequent oncogenic DNA damage may lead to the development of neoplasms. EBV-associated NK/T cell lymphoproliferative disorders are prevalent in Asia, but quite rare in Western countries. The genetic immunological background, therefore, is closely linked to the development of EBV-associated neoplasms.

AB - Epstein-Barr virus (EBV), or human herpesvirus 4 (HHV-4), infects the vast majority of adults worldwide, and establishes both nonproductive (latent) and productive (lytic) infections. Host immune responses directed against both the lytic and latent cycle-associated EBV antigens induce a diversity of clinical symptoms in patients with chronic active EBV infections who usually contain an oligoclonal pool of EBV-infected lymphocyte subsets in their blood. Episomal EBV genes in the latent infection utilize an array of evasion strategies from host immune responses: the minimized expression of EBV antigens targeted by host cytotoxic T lymphocytes (CTLs), the down-regulation of cell adhesion molecule expression, and the release of virokines to inhibit the host CTLs. The oncogenic role of latent EBV infection is not yet fully understood, but latent membrane proteins (LMPs) expressed during the latency cycle have essential biological properties leading to cellular gene expression and immortalization, and EBV-encoded gene products such as viral interleukin-10 (vIL-10) and bcl-2 homologue function to survive the EBV-infected cells. The subsequent oncogenic DNA damage may lead to the development of neoplasms. EBV-associated NK/T cell lymphoproliferative disorders are prevalent in Asia, but quite rare in Western countries. The genetic immunological background, therefore, is closely linked to the development of EBV-associated neoplasms.

KW - Chronic active EB virus infection

KW - Hemophagocytic syndrome

KW - Hydroa vacciniforme

KW - Latent infection

KW - Mosquito allergy

UR - http://www.scopus.com/inward/record.url?scp=4644319288&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4644319288&partnerID=8YFLogxK

M3 - Article

C2 - 15551754

AN - SCOPUS:4644319288

VL - 58

SP - 169

EP - 180

JO - Acta Medica Okayama

JF - Acta Medica Okayama

SN - 0386-300X

IS - 4

ER -