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Journal of Virology, May 2009, p. 4404-4411, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02657-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

JC Virus-Specific Immune Responses in Human Immunodeficiency Virus Type 1 Patients with Progressive Multifocal Leukoencephalopathy{triangledown}

Nina Khanna,1,2 Marcel Wolbers,3 Nicolas J. Mueller,4 Christian Garzoni,5 Renaud A. Du Pasquier,6 Christoph A. Fux,7 Pietro Vernazza,8 Enos Bernasconi,9 Raphael Viscidi,10 Manuel Battegay,1 Hans H. Hirsch,1,2* for the Swiss HIV Cohort Study

Division of Infectious Diseases and Hospital Epidemiology, University Hospital Basel, CH-4031 Basel, Switzerland,1 Institute for Medical Microbiology, Department of Biomedicine, University of Basel, CH-4003 Basel, Switzerland,2 Institute for Clinical Epidemiology and Biostatistics, University Hospital Basel, CH-4031 Basel, Switzerland,3 Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, CH-8091 Zurich, Switzerland,4 Division of Infectious Diseases and Laboratory of Virology, University Hospital Geneva, CH-1205 Geneva, Switzerland,5 Divisions of Neurology and Immunology, Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland,6 Division of Infectious Diseases, University Hospital and University of Bern, CH-3010 Bern, Switzerland,7 Department of Internal Medicine, Cantonal Hospital, CH-9000 St. Gallen, Switzerland,8 Department of Internal Medicine, Regional Hospital, CH-6900 Lugano, Switzerland,9 Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland,10

Received 24 December 2008/ Accepted 2 February 2009

Progressive multifocal leukoencephalopathy (PML) is a frequently fatal disease caused by uncontrolled polyomavirus JC (JCV) in severely immunodeficient patients. We investigated the JCV-specific cellular and humoral immunity in the Swiss HIV Cohort Study. We identified PML cases (n = 29), as well as three matched controls per case (n = 87), with prospectively cryopreserved peripheral blood mononuclear cells and plasma at diagnosis. Nested controls were matched according to age, gender, CD4+ T-cell count, and decline. Survivors (n = 18) were defined as being alive for >1 year after diagnosis. Using gamma interferon enzyme-linked immunospot assays, we found that JCV-specific T-cell responses were lower in nonsurvivors than in their matched controls (P = 0.08), which was highly significant for laboratory- and histologically confirmed PML cases (P = 0.004). No difference was found between PML survivors and controls or for cytomegalovirus-specific T-cell responses. PML survivors showed significant increases in JCV-specific T cells (P = 0.04) and immunoglobulin G (IgG) responses (P = 0.005). IgG responses in survivors were positively correlated with CD4+ T-cell counts (P = 0.049) and negatively with human immunodeficiency virus RNA loads (P = 0.03). We conclude that PML nonsurvivors had selectively impaired JCV-specific T-cell responses compared to CD4+ T-cell-matched controls and failed to mount JCV-specific antibody responses. JCV-specific T-cell and IgG responses may serve as prognostic markers for patients at risk.

* Corresponding author. Mailing address: Institute for Medical Microbiology, Department of Biomedicine, University of Basel, Petersplatz 10, CH-4003 Basel, Switzerland. Phone: 41 61 267-3262. Fax: 41 61 267-3283. E-mail: Hans.Hirsch{at}unibas.ch

{triangledown} Published ahead of print on 11 February 2009.

Journal of Virology, May 2009, p. 4404-4411, Vol. 83, No. 9
0022-538X/09/$08.00+0     doi:10.1128/JVI.02657-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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