Disease relevance of JC Virus

• Because of the low levels of Tst-1 present in oligodendrocytes, synergism between Tst-1 and T antigen could be an important factor in establishing the lytic infection of oligodendrocytes by JC virus during the course of the fatal demyelinating disease progressive multifocal leukoencephalopathy [1].
• The human polyomavirus JC virus (JCV) is the causative agent of a fatal demyelinating disease, progressive multifocal leukoencephalopathy, and encodes six major proteins, including agnoprotein [2].
• The human papovaviruses BK virus (BKV) and JC virus (JCV) both encode a large-tumor (T) antigen which are highly homologous to each other as well as to simian virus 40 (SV40) large-T antigen [3].
• The transcriptional control region of the human neurotropic polyomavirus JC virus contains a consensus NF-kappa B site which has been shown to enhance both basal and extracellular stimulus-induced levels of transcription of JC promoters [4].
• Analysis of capsid formation of human polyomavirus JC (Tokyo-1 strain) by a eukaryotic expression system: splicing of late RNAs, translation and nuclear transport of major capsid protein VP1, and capsid assembly [5].

Psychiatry related information on JC Virus

• With DNA extracted from brain specimens from 19 multiple sclerosis, 5 progressive multifocal leukoencephalopathy, 1 Alzheimer's disease, and 8 nonneurological control subjects, polymerase chain reaction was performed using nested sets of primer pairs amplifying segments of the large T and VP1 antigen-encoding sequences of JC virus [6].

High impact information on JC Virus

• The ability of pRb2/p130 to interact with JC virus T antigen was also studied [7].
• Cooperative action of cellular proteins YB-1 and Pur alpha with the tumor antigen of the human JC polyomavirus determines their interaction with the viral lytic control element [8].
• Brain vascular endothelial cells express JC virus large tumor antigen in immunocompetent and cyclophosphamide-treated hamsters [9].
• Because of its endogenous expression in myelinating glia, Tst-1/Oct-6 might also be an important determinant for the glia specificity of JC virus in vivo [10].
• JC virus DNA in the CSF and peripheral blood was quantified by kinetic polymerase chain reaction [11].

Chemical compound and disease context of JC Virus

• We here show that in situ PCR can detect JC virus in archival tissue sections of 3 cases of PML, including 1 of the original cases described in 1958 and 1 case that was fixed in formalin for 7 weeks [12].
• Differential distribution of the JC virus receptor-type sialic acid in normal human tissues [13].
• Stability and function of JC virus large T antigen and T' proteins are altered by mutation of their phosphorylated threonine 125 residues [14].
• Infection of glial cells by the human polyomavirus JC is mediated by an N-linked glycoprotein containing terminal alpha(2-6)-linked sialic acids [15].
• DNA:DNA in situ hybridization using a cloned JC virus (JCV) DNA probe labeled with biotin confirmed the presence of JCV DNA in formalin-fixed, paraffin-embedded brain biopsies from four cases of progressive multifocal leukoencephalopathy (PML) [16].

Biological context of JC Virus

• Detection of JC virus DNA sequences and expression of the viral regulatory protein T-antigen in tumors of the central nervous system [17].
• In conclusion, we demonstrate that JC virus Mad-1 and Delta98 are able to induce chromosomal instability in colonic cells with a hit and run mechanism that involves an early interaction with beta-catenin and p53 [18].
• Cell-specific activation of the glial-specific JC virus early promoter by large T antigen [19].
• Transcriptional activation of JC virus by human T-lymphotropic virus type I Tax protein in human neuronal cell lines [20].
• Interestingly, similar strong NFI-binding motifs were suggested to be present in the enhancer of JC virus whose gene is expressed like the MBP gene, in the nervous system [21].

Anatomical context of JC Virus

• Polymerase chain reaction performed on cerebrospinal fluid was positive for the JC virus (JC are the initials of the first person diagnosed with this virus) [22].

Gene context of JC Virus

• In demyelinated regions, both MAG and MBP staining were severely altered; also there was much less JC virus staining [23].
• In addition, competition for the IRS-1-T-antigen binding by a dominant negative mutant of IRS-1 inhibited growth and survival of JC virus T-antigen-transformed cells in anchorage-independent culture conditions [24].
• T-antigen of the human polyomavirus JC attenuates faithful DNA repair by forcing nuclear interaction between IRS-1 and Rad51 [25].
• Internalization of exogenous human immunodeficiency virus-1 protein, Tat, by KG-1 oligodendroglioma cells followed by stimulation of DNA replication initiated at the JC virus origin [26].
• This likely represents binding to, and prolongation of the half-life of, wild-type p53 protein by JC virus T-antigen [27].

Analytical, diagnostic and therapeutic context of JC Virus

• Molecular cloning and expression of major structural protein VP1 of the human polyomavirus JC virus: formation of virus-like particles useful for immunological and therapeutic studies [28].
• The diagnosis was documented by detecting and confirming sequences of SV40 (but not BK or JC virus) in his kidney biopsy and urine by polymerase chain reaction, Southern blot, and DNA sequencing [29].
• By polymerase chain reaction, JC virus (JCV) DNA was found in 6 of 7 patients at baseline but in only 1 patient after HAART [30].
• Using immunolabeling methods, the JC virus (JCV) early or regulatory protein, large T antigen, was demonstrated in frozen sections of neonatal hamster brains before tumor formation [31].
• Site-directed mutagenesis and gel shift analyses revealed that PMA and IL-1beta strongly induced nuclear factor-1 (NF-1) binding to the JC virus enhancer region, increasing transcriptional activity of the viral early promoter [32].

References