Contributions of E1A to mouse adenovirus type 1 pathogenesis following intranasal inoculation.

Journal Article (Journal Article)

We investigated the role of mouse adenovirus type 1 (MAV-1) early region 1A (E1A) protein in adenovirus respiratory infection. Intranasal (i.n.) inoculation of mice with wild type (wt) virus induced chemokine and cellular inflammatory responses in the lung. We observed similar responses in mice infected with an E1A-null mutant virus at the same dose, although the magnitude of these responses was lower. Levels of viral hexon gene expression were lower in the lung following infection with E1A-null virus than with wt virus. When input doses were adjusted so that equivalent viral loads were present following infection with varying doses of wt and E1A-null virus, we observed equivalent chemokine upregulation in the lung. Dissemination to the brain occurred following i.n. inoculation with equal doses of wt or E1A-null virus, but viral gene expression and viral loads were lower and the magnitude of chemokine responses was lower in brains of E1A-null virus-infected mice. CD4 and CD8 T cells and neutrophils were recruited to the brains of mice infected with either wt or E1A-null virus. Together, these data suggest that MAV-1 E1A makes important contributions to viral replication in the lung and the brain following i.n. inoculation. However, E1A is not essential for the induction of inflammatory responses in the lung or for viral dissemination out of the lung.

Full Text

Duke Authors

Cited Authors

  • Weinberg, JB; Jensen, DR; Gralinski, LE; Lake, AR; Stempfle, GS; Spindler, KR

Published Date

  • January 5, 2007

Published In

Volume / Issue

  • 357 / 1

Start / End Page

  • 54 - 67

PubMed ID

  • 16962154

Pubmed Central ID

  • PMC1764815

International Standard Serial Number (ISSN)

  • 0042-6822

Digital Object Identifier (DOI)

  • 10.1016/j.virol.2006.08.013


  • eng

Conference Location

  • United States