An outbreak of acute respiratory disease caused by a virus associated RNA II gene mutation strain of human adenovirus 7 in China, 2015

PLoS One. 2017 Feb 22;12(2):e0172519. doi: 10.1371/journal.pone.0172519. eCollection 2017.

Abstract

Human adenovirus 7 (HAdV-7) strains are a major cause of acute respiratory disease (ARD) among adults and children, associated with fatal pneumonia. An ARD outbreak caused by HAdV-7 that involved 739 college students was reported in this article. To better understand the underlying cause of this large-scale epidemic, virus strains were isolated from infected patients and sequence variations of the whole genome sequence were detected. Evolutionary trees and alignment results indicated that the major capsid protein genes hexon and fibre were strongly conserved among serotype 7 strains in China at that time. Instead, the HAdV-7 strains presented three thymine deletions in the virus associated RNA (VA RNA) II terminal region. We also found that the mutation might lead to increased mRNA expression of an adjacent gene, L1 52/55K, and thus promoted faster growth. These findings suggest that sequence variation of VA RNA II gene was a potential cause of such a severe HAdV-7 infection and this gene should be a new-emerging factor to be monitored for better understanding of HAdV-7 infection.

MeSH terms

  • Acute Disease
  • Adenovirus Infections, Human / epidemiology*
  • Adenovirus Infections, Human / virology*
  • Adenoviruses, Human / genetics*
  • Adolescent
  • China / epidemiology
  • Disease Outbreaks
  • Female
  • Genome, Viral
  • Humans
  • Male
  • Mutation
  • RNA / genetics*
  • Young Adult

Substances

  • RNA primers
  • RNA

Grants and funding

This work was supported by the Mega-projects of Science and Technology Research (nos. 2012ZX10004215 and AWS15J006) that received by HBS, who participated in study design and decision to publish. And the National Nature Science Foundation of China (nos. 81373053 and 81371854), and the Beijing Science and Technology Nova program (no. xx2013061) received by SFQ, who participated in study design and decision to publish.