Detection of JC virus DNA in the peripheral blood leukocytes of HIV-infected patients

Dubois, Vivien; Lafon, Marie‐Edith; Ragnaud, Jean‐Marie; Pellegrin, Jean‐Luc; Damasio, Francine; Baudouin, Christelle; Michaud, Vincent; Fleury, Hervé

doi:10.1097/00002030-199604000-00001

Cited by 55 publications

(43 citation statements)

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“…Peripheral blood leukocytes can be considered as the clinical material for the detection of these three organisms. However, detection of T. gondii, EBV and JCV in the blood is still difficult to interpret (29,30). In contrast to the high specificity of PCRin this study, we could not provide reliable data on the sensitivity of our PCR system because the number of positive cases was relatively small (five, five, and two for TE, PCNSL, and PML,respectively).…”

Section: Discussionmentioning

confidence: 77%

Detection of Toxoplasma gondii, Epstein-Barr Virus, and JC Virus DNAs in the Cerebrospinal Fluid in Acquired Immunodeficiency Syndrome Patients with Focal Central Nervous System Comlications.

et al. 1999

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Object Toxoplasmic encephalitis (TE), primary central nervous system lymphoma (PCNSL) and progressive multifocal leukoencephalopathy (PML) are major central nervous system (CNS) diseases in patients with acquired immunodeficiency syndrome (AIDS). Weassessed the diagnostic value of polymerase chain reaction (PCR) in the detection of DNAsof Toxoplasma gondii {T. gondii), Epstein-Barr virus (EBV) and JC virus (JCV) in the cerebrospinal fluid (CSF). Methods Wecompared the PCRresults with those of pathological findings at autopsy. Patients or Materials The present study included 23 autopsies representing those in whomCSF samples were obtained before death while the patient was hospitalized or at autopsy. Results The threshold levels for PCR detection were 4 tachyzoites of T. gondii, 5-15 genomes of EBVand 10 genomes of JCV. Weidentified T. gondii DNAin 4 out of5 autopsy-defined cases ofTE, EBVDNAin 5 out of5 cases with PCNSL, and JCV DNAin 2 out of2 cases with PML.The specificity ofPCR was 100% in TE, 78%in PCNSL, and 100% in PML. Conclusion Although the number of cases was relatively small in this study, PCRcorrectly identified T. gondii DNAin those cases in which PMLor PCNSL was the sole clinical diagnosis. Our results indicate that PCRexamination of CSFis a clinically useful tool for the diagnosis of focal brain lesions in patients with AIDS. (Internal Medicine 38: 556-562, 1999)

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Section: Discussionmentioning

confidence: 77%

Detection of Toxoplasma gondii, Epstein-Barr Virus, and JC Virus DNAs in the Cerebrospinal Fluid in Acquired Immunodeficiency Syndrome Patients with Focal Central Nervous System Comlications.

et al. 1999

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“…JCV is rarely found in the peripheral blood of normal persons (19,(21)(22)(23). JC viremia occurs in the setting of immunosuppression, and JCV DNA has been detected in the blood of HIV ϩ patients with or without PML who have CD4 ϩ cell counts below 200/l (19, 21, 24 -26).…”

Section: Resultsmentioning

confidence: 99%

Association of Prolonged Survival in HLA-A2+ Progressive Multifocal Leukoencephalopathy Patients with a CTL Response Specific for a Commonly Recognized JC Virus Epitope

Koralnik

Pasquier

Kuroda

et al. 2002

The Journal of Immunology

133

123

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The role of JC virus (JCV)-specific CTL was explored in the immunopathogenesis of progressive multifocal leukoencephalopathy (PML). We identified a 9-aa epitope of the JCV capsid protein VP1, the VP1p100 peptide ILMWEAVTL, which is recognized by CTL of HLA-A2+ HIV+/PML survivors. We then constructed an HLA-A*0201/VP1p100 tetrameric complex that allowed us to assess by flow cytometry the PBMC of 13 PML patients and 11 control subjects for the presence of JCV-specific CTL. VP1p100-specific CTL were detected by tetramer binding in VP1p100-stimulated PBMC of five of seven (71%) PML survivors and zero of six PML progressors (p = 0.02). Two of three HIV+ patients with a leukoencephalopathy resembling PML, but with no virologic evidence of JCV infection, also had detectable VP1p100-specific CTL in their PBMC. PBMC of eight HIV+ patients with other neurologic diseases and healthy control subjects had no detectable JCV-specific CTL. These data suggest that the JCV-specific cellular immune response may be important in the containment of PML, and the tetramer-staining assay may provide a useful prognostic tool in the clinical management of these patients.

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“…The polyomavirus JC virus (JCV) is a ubiquitous human pathogen (21,25,32) that is initially subclinical yet establishes a persistent infection in the kidney (11). In immunosuppressed individuals JCV can become reactivated, leading to infection in the central nervous system (CNS) (13)(14)(15)20), where the virus specifically targets glial cells, including astrocytes and the myelin-producing cells, oligodendrocytes (40,48). JCV infection and cytolytic destruction of oligodendroglia cause the fatal disease progressive multifocal leukoencephalopathy (PML) (1, 22).…”

Section: Jc Virus (Jcv) Is a Human Polyomavirus And The Causative Agementioning

confidence: 99%

Role of N-Linked Glycosylation of the 5-HT _2A Receptor in JC Virus Infection

Maginnis

Haley

Gee

et al. 2010

J Virol

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JC virus (JCV) is a human polyomavirus and the causative agent of the fatal demyelinating disease progressive multifocal leukoencephalopathy (PML). JCV infection of host cells is dependent on interactionsThe initial interaction between virus and host occurs via molecular interactions of viral attachment proteins and receptors on host cells. Therefore, receptor recognition is a critical host cell determinant and may play a key regulatory role in viral pathogenesis. The polyomavirus JC virus (JCV) is a ubiquitous human pathogen (21,25,32) that is initially subclinical yet establishes a persistent infection in the kidney (11). In immunosuppressed individuals JCV can become reactivated, leading to infection in the central nervous system (CNS) (13)(14)(15)20), where the virus specifically targets glial cells, including astrocytes and the myelin-producing cells, oligodendrocytes (40,48). JCV infection and cytolytic destruction of oligodendroglia cause the fatal disease progressive multifocal leukoencephalopathy (PML) (1, 22). The most common cause of PML is associated with human immunodeficiency virus (HIV) and AIDS (10, 23). However, in recent years PML has been reported in patients receiving immunosuppressive therapies for autoimmune diseases such as Crohn's disease (44), multiple sclerosis (MS) (24,26,28,47), systemic lupus erythematosus (5, 33), and rheumatoid arthritis (5, 19, 37). The prognosis of PML is bleak, as the disease progresses rapidly and usually proves fatal within 1 year of the onset of symptoms. While current treatment options for PML are limited (23), recent studies suggest that mirtazapine, a serotonin receptor antagonist, may be capable of slowing the progression of PML (6,27,45,46). JCV has a nonenveloped, icosahedral capsid that encapsidates a circular double-stranded DNA (dsDNA) genome (39). JCV attachment to cells is mediated by an N-linked glycoprotein with either ␣(2,3)-or ␣(2,6)-linked sialic acid (16, 31), suggesting that N-linked glycosylation of cellular receptors is important for JCV infection. N-linked glycosylation is a posttranslational process by which oligosaccharides are added to asparagine residues, and this modification is important for protein processing, folding, expression, and function (43). Previous studies from our laboratory revealed that the JCV also requires the serotonin 5-hydroxytryptamine 2A receptor (5-HT 2A R) to mediate JCV infection (18,35,38), while others report that JCV infection can occur in the absence of 5-HT 2A R (7,8). 5-HT 2A R is a seven-transmembrane-spanning G-protein-coupled receptor that belongs to a large family of 5-HT serotonin receptors. 5-HT 2A R is abundantly expressed on cells in the brain (4), including glial cells (3), and in the kidney (4), which parallels the sites of JCV infection. N-linked glycosylation plays a key regulatory role in the function of serotonin receptors. Mutation of N-linked glycosylation sites in human 5-HT 3A R and 5-HT 5A R results in decreased expression at the plasma membrane, which is critical for receptor functio...

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Detection of JC virus DNA in the peripheral blood leukocytes of HIV-infected patients

Cited by 55 publications

References 0 publications

Detection of Toxoplasma gondii, Epstein-Barr Virus, and JC Virus DNAs in the Cerebrospinal Fluid in Acquired Immunodeficiency Syndrome Patients with Focal Central Nervous System Comlications.

Detection of Toxoplasma gondii, Epstein-Barr Virus, and JC Virus DNAs in the Cerebrospinal Fluid in Acquired Immunodeficiency Syndrome Patients with Focal Central Nervous System Comlications.

Association of Prolonged Survival in HLA-A2+ Progressive Multifocal Leukoencephalopathy Patients with a CTL Response Specific for a Commonly Recognized JC Virus Epitope

Role of N-Linked Glycosylation of the 5-HT _2A Receptor in JC Virus Infection

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Detection of JC virus DNA in the peripheral blood leukocytes of HIV-infected patients

Cited by 55 publications

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Detection of Toxoplasma gondii, Epstein-Barr Virus, and JC Virus DNAs in the Cerebrospinal Fluid in Acquired Immunodeficiency Syndrome Patients with Focal Central Nervous System Comlications.

Detection of Toxoplasma gondii, Epstein-Barr Virus, and JC Virus DNAs in the Cerebrospinal Fluid in Acquired Immunodeficiency Syndrome Patients with Focal Central Nervous System Comlications.

Association of Prolonged Survival in HLA-A2+ Progressive Multifocal Leukoencephalopathy Patients with a CTL Response Specific for a Commonly Recognized JC Virus Epitope

Role of N-Linked Glycosylation of the 5-HT 2A Receptor in JC Virus Infection

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Role of N-Linked Glycosylation of the 5-HT _2A Receptor in JC Virus Infection