scholarly journals JC Virus Antibody and Viremia as Predictors of Progressive Multifocal Leukoencephalopathy in Human Immunodeficiency Virus-1–Infected Individuals

2011 ◽  
Vol 53 (7) ◽  
pp. 711-715 ◽  
Author(s):  
Raphael P. Viscidi ◽  
Nina Khanna ◽  
Chen S. Tan ◽  
Xiuhung Li ◽  
Lisa Jacobson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Jc Virus ◽  
Virus Antibody ◽  
Immunodeficiency Virus ◽  
Human Immunodeficiency Virus 1

Evidence for Involvement of Transforming Growth Factor β1 Signaling Pathway in Activation of JC Virus in Human Immunodeficiency Virus 1–Associated Progressive Multifocal Leukoencephalopathy

2004 ◽  
Vol 128 (3) ◽  
pp. 282-291
Author(s):  
Sahnila Enam ◽  
Thersa M. Sweet ◽  
Shohreh Amini ◽  
Kamel Khalili ◽  
Luis Del Valle
Keyword(s):  
Human Immunodeficiency Virus ◽  
Growth Factor ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Transforming Growth Factor ◽  
Jc Virus ◽  
Transforming Growth Factor Β1 ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Human Immunodeficiency Virus 1

Abstract Context.—Progressive multifocal leukoencephalopathy is a fatal demyelinating disease of the central nervous system frequently seen in patients with impaired immune systems, particularly acquired immunodeficiency syndrome. JC virus (JCV), a human neurotropic polyomavirus, is the etiologic infectious agent of this disease. Objective.—The significantly higher incidence of progressive multifocal leukoencephalopathy in patients with acquired immunodeficiency syndrome than in patients with other immunosuppressive conditions suggests that molecular interactions between human immunodeficiency virus 1 and JCV, via the Tat protein, are responsible for the activation of the JCV enhancer/promoter and the development of progressive multifocal leukoencephalopathy. An indirect mechanism through activation of cytokines, such as transforming growth factor β1 and Smads 3 and 4, may also be responsible for the enhancement of JCV gene expression. Design.—Immunohistochemical analysis in progressive multifocal leukoencephalopathy samples and chloramphenicol acetyl transferase assays on cell cultures were performed to corroborate this hypothesis. Results.—The JCV capsid protein VP-1 was found in the nuclei of oligodendrocytes and in the nuclei and cytoplasm of bizarre astrocytes. Human immunodeficiency virus proteins, including p24 and Tat, were detected in the cytoplasm of astrocytes. Tat, but not p24, was detected in oligodendrocytes, suggesting that extracellular Tat accumulates in the nuclei of oligodendrocytes, where JCV gene transcription takes place. High levels of transforming growth factor β1 and Smads 3 and 4 were detected in JCV-infected oligodendrocytes. Results from in vitro studies confirm activation of the JCV early and late promoters by Smads 3 and 4. Conclusions.—These observations support our model, suggesting that the induction of transforming growth factor β1 by human immunodeficiency virus 1 Tat can stimulate its downstream factors, including Smads 3 and 4, which in turn augment transcription of the JCV promoter in glial cells.

scholarly journals JC virus/human immunodeficiency virus 1 co-infection in the Brazilian Amazonian region

2016 ◽  
Vol 20 (4) ◽  
pp. 360-364 ◽  
Author(s):  
Izaura Maria Vieira Cayres-Vallinoto ◽  
Antonio Carlos Rosário Vallinoto ◽  
Giselle Priscila dos Anjos Pena ◽  
Vânia Nakauth Azevedo ◽  
Luiz Fernando Almeida Machado ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Jc Virus ◽  
Immunodeficiency Virus ◽  
Amazonian Region ◽  
Human Immunodeficiency Virus 1

Exogenous human immunodeficiency virus-1 protein, tat, enhances replication of JC virus efficiently in neuroblastoma cell lines

2012 ◽  
Vol 84 (4) ◽  
pp. 555-561 ◽  
Author(s):  
Souichi Nukuzuma ◽  
Masanori Kameoka ◽  
Shigeki Sugiura ◽  
Kazuo Nakamichi ◽  
Chiyoko Nukuzuma ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cell Lines ◽  
Jc Virus ◽  
Neuroblastoma Cell ◽  
Immunodeficiency Virus ◽  
Neuroblastoma Cell Lines ◽  
Human Immunodeficiency Virus 1

scholarly journals JC Virus-Specific Immune Responses in Human Immunodeficiency Virus Type 1 Patients with Progressive Multifocal Leukoencephalopathy

2009 ◽  
Vol 83 (9) ◽  
pp. 4404-4411 ◽  
Author(s):  
Nina Khanna ◽  
Marcel Wolbers ◽  
Nicolas J. Mueller ◽  
Christian Garzoni ◽  
Renaud A. Du Pasquier ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Mononuclear Cells ◽  
Jc Virus ◽  
T Cell Responses ◽  
Peripheral Blood Mononuclear ◽  
Cell Responses ◽  
Cell Counts ◽  
Immunodeficiency Virus

ABSTRACT 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.

scholarly journals JC Virus Granule Cell Neuronopathy as AIDS-Presenting Illness

2018 ◽  
Vol 45 (4) ◽  
pp. 466-469 ◽  
Author(s):  
Simon Grandjean Lapierre ◽  
Xin Dang ◽  
Danielle Gilbert ◽  
Sylvie Lauzier ◽  
Igor J. Koralnik ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Virus Infection ◽  
Human Immunodeficiency Virus Infection ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Granule Cell ◽  
Demyelinating Disease ◽  
Jc Virus ◽  
Clinical Manifestations ◽  
Immunodeficiency Virus ◽  
Granule Cell Neuronopathy

AbstractJC virus is the etiological agent of progressive multifocal leukoencephalopathy, a white matter demyelinating disease that mostly affects immunocompromised patients. JC virus can also infect neurons and meningeal cells and cause encephalitis, meningitis and granule cell neuronopathy. We report a patient with JC virus granule cell neuronopathy, without concomitant progressive multifocal leukoencephalopathy, presenting as inaugural acquired immune deficiency syndrome-related illness. This patient’s human immunodeficiency virus infection remained undiagnosed for several months after neurological symptoms onset. We review JC virus pathophysiology, clinical manifestations, treatment and prognosis, and emphasize the importance of considering human immunodeficiency virus infection and related opportunistic infections in the differential diagnosis of new-onset isolated cerebellar disease.

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