This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by KLAVINSKIS, L. S. Articles by OLDSTONE, M. B. A. Search for Related Content PubMed PubMed Citation Articles by KLAVINSKIS, L. S. Articles by OLDSTONE, M. B. A. Pubmed/NCBI databases Substance via MeSH Hazardous Substances DB THYROGLOBULIN

Persistent Viral Infection of the Thyroid Gland: Alteration of Thyroid Function in the Absence of Tissue Injury^*

LINDA S. KLAVINSKIS, ABNER L. NOTKINS and MICHAEL B. A. OLDSTONE

Scripps Clinic and Research Foundation La Jolla, California 92037
The Laboratory of Oral Medicine, National Institutes of Dental Research, National Institutes of Health (A.L.N.) Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: Dr. Linda S. Klavinskis, Department of Immunology, Research Institute of Scripps Clinic, 10666 North Torrey Pines Road, La Jolla, California 92037.

Abstract

The possible role of viruses as the cause of some thyroid disorders was evaluated in three strains of mice neonatally infected with lymphocytic choriomeningitis virus. We report the first definitive evidence that viruses can persist in the thyroid gland, particularly thyroid epithelial cells in which thyroglobulin is synthesized. Concomitant with the infection of these cells was a significant reduction in the level of thyroglobulin mRNA and circulating thyroid hormones. Another virus that causes persistent infection but does not replicate in the thyroid gland failed to alter serum levels of thyroid hormones, indicating the thyroid dysfunction was not a generalized result of stress accompanying a persistent infection. This alteration in thyroid homeostasis during persistent infection with lymphocytic choriomeningitis virus is not caused by autoantibodies to the thyroid. Moreover, despite infection of the thyroid gland, neither necrosis nor inflammation occurs. Thyroid dysfunction was noted both when persistence was initiated at birth and in utero during congenital infection. These observations in an experimental model raise the issue that viruses may play a role in the pathogenesis of some thyroid disorders in man. (Endocrinology 122: 567–575, 1988)

Footnotes

^* This is publication 4551-IMM from the Department of Immunology, Research Institute of Scripps Clinic (La Jolla, CA). This work was supported by USPHS Grant AG-04342.

Recipient of a Fulbright Traveling Scholarship and Wellcome Travel Grant.

Received March 19, 1987.

This article has been cited by other articles:

				K. Yamazaki, K. Suzuki, E. Yamada, T. Yamada, F. Takeshita, M. Matsumoto, T. Mitsuhashi, T. Obara, K. Takano, and K. Sato Suppression of Iodide Uptake and Thyroid Hormone Synthesis with Stimulation of the Type I Interferon System by Double-Stranded Ribonucleic Acid in Cultured Human Thyroid Follicles Endocrinology, July 1, 2007; 148(7): 3226 - 3235. [Abstract] [Full Text] [PDF]

				V. P. Rao, A. E. Kajon, K. R. Spindler, and G. Carayanniotis Involvement of Epitope Mimicry in Potentiation But Not Initiation of Autoimmune Disease J. Immunol., May 15, 1999; 162(10): 5888 - 5893. [Abstract] [Full Text] [PDF]