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WU Polyomavirus in Respiratory Epithelial Cells from Lung Transplant Patient with Job Syndrome - Volume 21, Number 1—January 2015 - Emerging Infectious Disease journal - CDC

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WU Polyomavirus in Respiratory Epithelial Cells from Lung Transplant Patient with Job Syndrome - Volume 21, Number 1—January 2015 - Emerging Infectious Disease journal - CDC


Volume 21, Number 1—January 2015


WU Polyomavirus in Respiratory Epithelial Cells from Lung Transplant Patient with Job Syndrome

Erica A. Siebrasse, Diana V. Pastrana, Nang L. Nguyen, Annie Wang, Mark J. Roth, Steven M. Holland, Alexandra F. Freeman, John McDyer, Christopher B. Buck, and David WangComments to Author 
Author affiliations: Washington University School of Medicine, St. Louis, Missouri, USA (E.A. Siebrasse, N.L. Nguyen, A. Wang, D. Wang)National Institutes of Health, Bethesda, Maryland, USA (D.V. Pastrana, M.J. Roth, S.M. Holland, A.F. Freeman, C.B. Buck)University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA (J. McDyer)


We detected WU polyomavirus (WUPyV) in a bronchoalveolar lavage sample from lungs transplanted into a recipient with Job syndrome by using immunoassays specific for the WUPyV viral protein 1. Co-staining for an epithelial cell marker identified most WUPyV viral protein 1–positive cells as respiratory epithelial cells.
WU polyomavirus (WUPyV) was discovered in a child with pneumonia in 2007 (1). Subsequent studies showed that WUPyV infection is common (24), and viral DNA can be detected in a variety of specimen types, including respiratory tract secretions (5). However, the virus has yet to be associated with any disease, and the specific cell type(s) infected by WUPyV has not been identified. Other human polyomaviruses are known pathogens, which typically cause disease in the context of immunosuppression (68).
Job syndrome is an immune disorder characterized by eczematoid dermatitis, recurrent skin and pulmonary infections, increased levels of IgE, and impaired T and B cell memory (9). This disorder is caused by dominant-negative mutations in the STAT3 gene (9). We report WUPyV cell tropism in lungs transplanted into a recipient with Job syndrome.

Ms. Siebrasse is a graduate student at Washington University, St. Louis, Missouri. Her research interests focus on discovery and characterization of novel polyomaviruses.


We thank Kenneth N. Olivier and Erika Crouch for help with interpretation of the slides, Peter C. FitzGerald for assistance with the bioinformatics analysis, and Patti Fetsch for immunocytochemical staining of SV40.
Experimental support was provided by the Hybridoma Facility of the Rheumatic Diseases Core Center. This study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH (award no. P30AR048335); the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH; grant R21AI095922 to D.W.; the Children’s Discovery Institute at Washington University in St. Louis; and the NIH Intramural Research Program, with support from the Center for Cancer Research and National Institute of Allergy and Infectious Diseases. E.A.S. was supported by the Department of Defense through the National Defense Science and Engineering Graduate Fellowship Program.


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Suggested citation for this article: Siebrasse EA, Pastrana DV, Nguyen NL, Wang A, Roth MJ, Holland SM, et al. WU polyomavirus in respiratory epithelial cells from lung transplant patient with Job syndrome. Emerg Infect Dis [Internet]. 2015 Jan [date cited]. http://dx.doi.org/10.3201/eid2101.140855
DOI: 10.3201/eid2101.140855

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