Previous Article | Next Article ![]()
Infection and Immunity, June 2005, p. 3794-3798, Vol. 73, No. 6
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.6.3794-3798.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Lisa M. McGinnis,1
Katharine C. Madigan,1,
Ping Cao,2
Timothy L. Cover,2,4
George W. Liechti,1
Richard M. Peek Jr.,3,4 and
Mark H. Forsyth1*
The College of William and Mary, Department of Biology, Williamsburg, Virginia 23187-8795,1 Vanderbilt University School of Medicine, Division of Infectious Diseases, Departments of Medicine and Microbiology and Immunology, Nashville, Tennessee 37232-2279,2 Vanderbilt University School of Medicine, Department of Medicine, Division of Gastroenterology, and Department of Cancer Biology, Nashville, Tennessee 37232-2279,3 Department of Veterans Affairs Medical Center, Nashville, Tennessee 372124
Received 22 September 2004/ Returned for modification 20 December 2004/ Accepted 7 February 2005
In an analysis of Helicobacter pylori genomic DNA by macroarray methodology, genomic DNA from a panel of cag pathogenicity island (PAI)-negative H. pylori clinical isolates failed to hybridize with 27 genes located outside the cag PAI in a cag PAI-positive reference strain. PCR analyses confirmed that HP0217 (encoding a lipopolysaccharide biosynthetic protein) and HP1079 (encoding a protein of unknown function) were present significantly more frequently in cagA-positive strains than in cagA-negative strains. A low G+C content of these two genes suggests they were acquired by horizontal transfer events.
Present address: University of Virginia School of Medicine, Charlottesville, VA 22908.
Present address: Thomas Jefferson University, Jefferson Medical College, Philadelphia, PA 19107.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»