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Human Parvovirus B19 Transgenic Mice Become Susceptible to Polyarthritis¹

Naruhiko Takasawa^*, Yasuhiko Munakata^*, Keiko Kumura Ishii^*, Yuichi Takahashi^*, Minako Takahashi^*, Yi Fu^*, Tomonori Ishii^*, Hiroshi Fujii^*, Takako Saito^*, Hiroshi Takano, Tetsuo Noda, Misao Suzuki, Masato Nose, Suzan Zolla-Patzner^¶ and Takeshi Sasaki^2,*

Departments of ^* Rheumatology and Hematology and Molecular Genetics, Tohoku University Graduate School of Medicine, Sendai, Japan; Center for Animal Resources and Development of Kumamoto University, Kumamoto, Japan; Department of Pathology, Ehime University School of Medicine, Ehime, Japan; and ^¶ Department of Pathology, New York University Medical School, New York, NY 10016

Human parvovirus B19 (B19) often causes acute polyarthritis in adults. In this paper, we analyzed nucleotide sequences of the B19 genome of patients with rheumatoid arthritis (RA), and then introduced the nonstructual protein 1 (NS1) gene of B19 into C57BL/6 mice that had a genetic origin not susceptible to arthritis. The transgenic mice developed no lesions spontaneously, but were susceptible to type II collagen (CII)-induced arthritis. B19 NS1 was expressed in synovial cells on the articular lesions that were histologically characteristic of granulomatous synovitis and pannus formation in cartilage and bone. Serum levels of anti-CII Abs and TNF- increased in NS1 transgenic mice to the same levels as those of DBA/1 mice, which were susceptible to polyarthritis. Stimulation with CII increased secretion of Th1-type- and Th2-type cytokines in NS1 transgenic mice, indicating that a nonpermissive H-2^b haplotype in the wild type of C57BL/6 mice can be made susceptible to polyarthritis through the expression of NS1. This study is the first to show that a viral agent from the joints in humans can cause CII-induced arthritis resembling RA.