Inherited chromosomally integrated human herpesvirus 6 and autoimmune connective tissue diseases.


Journal

Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
ISSN: 1873-5967
Titre abrégé: J Clin Virol
Pays: Netherlands
ID NLM: 9815671

Informations de publication

Date de publication:
11 2020
Historique:
received: 15 06 2020
revised: 27 09 2020
accepted: 03 10 2020
pubmed: 13 10 2020
medline: 18 9 2021
entrez: 12 10 2020
Statut: ppublish

Résumé

Entire genome of human herpesvirus 6 (HHV-6) that integrates into human chromosomes is called chromosomally integrated HHV-6 (ciHHV-6). Several viral infections have been suggested to be involved in autoimmune connective tissue diseases (CTDs). Reactivated HHV-6 from the integrated viral genome can induce immune responses against the virus. Thus, it is plausible that ciHHV-6 is associated with autoimmune CTDs. We sought to determine whether the prevalence of ciHHV-6 was significantly higher in patients with autoimmune CTDs than in a healthy population. A total of 846 peripheral blood samples collected from autoimmune CTD patients were analyzed. Since there was a large number of samples, they were pooled into 24 samples per group. Copy numbers of HHV-6 DNA were measured by real-time PCR. The threshold level for distinguishing between ciHHV-6 and active viral infection and the reliability of pooled DNA analysis were examined as initial validation experiments. The threshold level was 1.6 × 10^6 copy/mL in whole blood. The reliability of pooled DNA analysis to identify one ciHHV-6 sample among 23 HHV-6 DNA-negative samples was high. No HHV-6 DNA was detected in any of the pooled DNA samples collected from the patients. The probability of the present study including the 846 autoimmune CTD patient's samples was statistically not different with a healthy Japanese population which was 0.2 % or 0.6 %. There was no significant difference in the prevalence of ciHHV-6 between a healthy population and patients with autoimmune CTDs.

Sections du résumé

BACKGROUND
Entire genome of human herpesvirus 6 (HHV-6) that integrates into human chromosomes is called chromosomally integrated HHV-6 (ciHHV-6). Several viral infections have been suggested to be involved in autoimmune connective tissue diseases (CTDs). Reactivated HHV-6 from the integrated viral genome can induce immune responses against the virus. Thus, it is plausible that ciHHV-6 is associated with autoimmune CTDs.
OBJECTIVES
We sought to determine whether the prevalence of ciHHV-6 was significantly higher in patients with autoimmune CTDs than in a healthy population.
STUDY DESIGN
A total of 846 peripheral blood samples collected from autoimmune CTD patients were analyzed. Since there was a large number of samples, they were pooled into 24 samples per group. Copy numbers of HHV-6 DNA were measured by real-time PCR. The threshold level for distinguishing between ciHHV-6 and active viral infection and the reliability of pooled DNA analysis were examined as initial validation experiments.
RESULTS
The threshold level was 1.6 × 10^6 copy/mL in whole blood. The reliability of pooled DNA analysis to identify one ciHHV-6 sample among 23 HHV-6 DNA-negative samples was high. No HHV-6 DNA was detected in any of the pooled DNA samples collected from the patients. The probability of the present study including the 846 autoimmune CTD patient's samples was statistically not different with a healthy Japanese population which was 0.2 % or 0.6 %.
CONCLUSIONS
There was no significant difference in the prevalence of ciHHV-6 between a healthy population and patients with autoimmune CTDs.

Identifiants

pubmed: 33045641
pii: S1386-6532(20)30398-X
doi: 10.1016/j.jcv.2020.104656
pii:
doi:

Substances chimiques

DNA, Viral 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

104656

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Yoshiki Kawamura (Y)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Aichi, Japan. Electronic address: yoshiki@fujita-fujita.ac.jp.

Takako Hashimoto (T)

Division of Rheumatology, Department of Internal Medicine, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Hiroki Miura (H)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Kei Kozawa (K)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Akiko Yoshikawa (A)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Naomi Ikeda (N)

Division of Rheumatology, Department of Internal Medicine, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Hiroshi Yatsuya (H)

Department of Public Health, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Hidekata Yasuoka (H)

Division of Rheumatology, Department of Internal Medicine, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

Tetsushi Yoshikawa (T)

Department of Pediatrics, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.

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