BK-Related Polyomavirus Vasculopathy in a Renal-Transplant Recipient
Tina Petrogiannis-Haliotis, M.D., Ph.D., George Sakoulas, M.D., James Kirby, M.D., Ph.D., Igor J. Koralnik, M.D., Ann M. Dvorak, M.D., Rita Monahan-Earley, Paola C. De Girolami, M.D., Umberto De Girolami, M.D., Melissa Upton, M.D., Eugene O. Major, Ph.D., Luz-Andrea Pfister, M.D., and Jeffrey T. Joseph, M.D., Ph.D.
Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.
Polyomaviruses typically infect a single species and limitedtypes of tissue. Examples include the human BK and JC virusesand simian virus 40 (SV40). These three viruses are approximately70 percent homologous with each other. They are nonenvelopedviruses with a circular, double-stranded–DNA genome of5 kb and a virion with a diameter of 45 nm.1 Their genome hasan early region encoding the large T and small t proteins, alate region encoding viral capsid proteins, and a noncodingregulatory region.
Primary infection with BK or JC virus usually occurs in childhoodand is asymptomatic. More than 80 percent . . . [Full Text of this Article]
Case Report
Methods
Results
Discussion
Source Information
From the Department of Pathology (T.P.-H., J.K., A.M.D., R.M.-E., P.C.D., M.U., J.T.J.), the Division of Infectious Diseases, Department of Internal Medicine (G.S.), the Division of Viral Pathogenesis (I.J.K., L.-A.P.), and the Department of Neurology (I.J.K., J.T.J.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston; the Division of Neuropathology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston (U.D.); and the Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, Bethesda, Md. (E.O.M.).
Address reprint requests to Dr. Joseph at the Department of Neurology, KS418, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02115, or at jjoseph@caregroup.harvard.edu.
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