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Open Access Research article

No evidence of a death-like function for species B1 human adenovirus type 3 E3-9K during A549 cell line infection

Kathryn M Frietze13, Samuel K Campos2 and Adriana E Kajon1*

Author Affiliations

1 Infectious Disease Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM, USA

2 Department of Immunobiology, BIO5 Institute, University of Arizona, Keating Building Rm 423, 1657 E. Helen St, Tucson, 85721-0240, AZ, USA

3 Department of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, NM, 87131-0001, USA

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BMC Research Notes 2012, 5:429  doi:10.1186/1756-0500-5-429

Published: 11 August 2012

Abstract

Background

Subspecies B1 human adenoviruses (HAdV-B1) are prevalent respiratory pathogens. Compared to their species C (HAdV-C) counterparts, relatively little work has been devoted to the characterization of their unique molecular biology. The early region 3 (E3) transcription unit is an interesting target for future efforts because of its species-specific diversity in genetic content among adenoviruses. This diversity is particularly significant for the subset of E3-encoded products that are membrane glycoproteins and may account for the distinct pathobiology of the different human adenovirus species. In order to understand the role of HAdV-B-specific genes in viral pathogenesis, we initiated the characterization of unique E3 genes. As a continuation of our efforts to define the function encoded in the highly polymorphic ORF E3-10.9K and testing the hypothesis that the E3-10.9K protein orthologs with a hydrophobic domain contribute to the efficient release of viral progeny, we generated HAdV-3 mutant viruses unable to express E3-10.9K ortholog E3-9K and examined their ability to grow, disseminate, and egress in cell culture.

Results

No differences were observed in the kinetics of infected cell death, and virus progeny release or in the plaque size and dissemination phenotypes between cells infected with HAdV-3 E3-9K mutants or the parental virus. The ectopic expression of E3-10.9K orthologs with a hydrophobic domain did not compromise cell viability.

Conclusions

Our data show that despite the remarkable similarities with HAdV-C E3-11.6K, HAdV-B1 ORF E3-10.9K does not encode a product with a “death-like” biological activity.

Keywords:
Adenovirus; E3 region; Genetic polymorphism; Virus egress