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Clinical and Diagnostic Laboratory Immunology, May 1999, p. 330-335, Vol. 6, No. 3
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

RNAs in the Sera of Persian Gulf War Veterans Have Segments Homologous to Chromosome 22q11.2

Howard B. Urnovitz,1,* James J. Tuite,1 Jean M. Higashida,2 and William H. Murphy3

Chronic Illness Research Foundation, Berkeley, California1; Division of Rheumatology, Veterans Affairs, Northern California Health Care System, Martinez, California2; and The University of Michigan School of Medicine, Ann Arbor, Michigan3

Received 15 October 1998/Returned for modification 4 December 1998/Accepted 25 February 1999

Reverse transcriptase PCR (RT-PCR) was used for polyribonucleotide assays with sera from deployed Persian Gulf War veterans with the Gulf War Syndrome and a cohort of nonmilitary controls. Sera from veterans contained polyribonucleotides (amplicons) that were obtained by RT-PCR and that ranged in size from 200 to ca. 2,000 bp. Sera from controls did not contain amplicons larger than 450 bp. DNA sequences were derived from two amplicons unique to veterans. These amplicons, which were 414 and 759 nucleotides, were unrelated to each other or to any sequence in gene bank databases. The amplicons contained short segments that were homologous to regions of chromosome 22q11.2, an antigen-responsive hot spot for genetic rearrangements. Many of these short amplicon segments occurred near, between, or in chromosome 22q11.2 Alu sequences. These results suggest that genetic alterations in the 22q11.2 region, possibly induced by exposures to environmental genotoxins during the Persian Gulf War, may have played a role in the pathogenesis of the Gulf War Syndrome. However, the data did not exclude the possibility that other chromosomes also may have been involved. Nonetheless, the detection of polyribonucleotides such as those reported here may have application to the laboratory diagnosis of chronic diseases that have a multifactorial etiology.

* Corresponding author. Mailing address: 1440 Fourth St., Berkeley, CA 94710. Phone: (510) 749-5100. Fax: (510) 526-5381. E-mail: hervdoc{at}aol.com.

Clinical and Diagnostic Laboratory Immunology, May 1999, p. 330-335, Vol. 6, No. 3
1071-412X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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