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PubMed1987

Surface antigens on hamster cells transformed by SV40, BK virus and JC virus.

We studied the surface antigens on hamster cells transformed by SV40, BK and JC viruses using a complement-dependent cytotoxicity test. Antiserum was obtained from guinea pigs immunized with an SV40-transformed hamster cell line, and used after appropriate absorption with a range of cell types. The cell lines transformed by these viruses were all found to possess the following surface antigens: 1) a unique set of organ antigens, 2) fetal antigen(s), and 3) an antigen tentatively named primate polyoma virus-transformed hamster cell antigen (PPH antigen-1). These antigens were not detected on other hamster cell lines, including those transformed by mouse polyoma-, adeno-, herpes-, or retro-viruses Neither could they be detected on mouse, rat or human cells transformed by SV40 or BK viruses. They were, thus, probably host-derived antigens specifically depressed or unmasked by the primate polyoma viruses. In addition, all hamster cell lines tested, including BHK21, carried an antigen(s) named hamster cell line antigen, which could not be detected on surfaces of normal cells, in primary or secondary culture.

Animals↗
PubMed1994

Nested PCR for detection of BK virus and JC virus DNA.

BACKGROUND: A nested polymerase chain reaction (PCR) was developed to detect BK virus (BKV) and JC virus (JCV) DNA sequences. The unique clevage site for BamHI restriction enzyme was located in teh JCV amplimer and cleavage was used to differentiate between BKV and JCV. STUDY DESIGN: Twenty-three urine specimens from 17 bone marrow recipients with haemorrhagic cystitis and one liver transplant patient were tested for the presence of BKV and JCV DNA. Four brain tissue specimens (paraffin embedded brain tissues and a fresh frozen brain biopsy) and 5 cerebrospinal fluids from 3 AIDS patients and one liver transplant patient, all with progressive multifocal leukoencephalopathy (PML), were also examined by PCR. RESULTS: The sensitivity of the PCR was 10 genomes for each virus. BKV DNA was detected in 15 urine specimens from 12 bone marrow transplant patients. JCV DNA was detected in 4 cerebrospinal fluids and 4 brain tissues from patients with PML. CONCLUSION: Our results show that the nested PCR is a sensitive and rapid assay that can be used for diagnosis of BKV and JCV infections.

Journal Article↗
PubMed2006

Cross-reactive CTL recognizing two HLA-A*02-restricted epitopes within the BK virus and JC virus VP1 polypeptides are frequent in immunocompetent individuals.

Two HLA-A*02-restricted epitopes have been identified within the VP1 polypeptide of a human polyomavirus, BK virus, which is associated with polyomavirus-associated nephropathy in kidney transplant patients. Immunization of transgenic mice with recombinant modified vaccinia Ankara expressing BKV VP1 (rMVA-BKV VP1) elicited functional CTL populations recognizing the sequences LLMWEAVTV (amino acids residues 108-116, BKV VP1p108) and AITEVECFL (residues 44-52, BKV VP1p44) and cross-reactive to the previously described JC virus VP1 homologs. Flow-based analyses of PBMC from a panel of thirty healthy HLA-A*02 human volunteers indicated that the majority of these subjects harbored functional CTL populations recognizing the BKV epitopes and cross-reactive with the JCV homologs. CTL recognizing the JCV VP1p100 and JCV VP1p36 epitopes have previously been associated with prolonged survival in progressive multifocal leukoencephalopathy patients. These findings suggest that infection with BKV or JCV could potentially induce cross-protective T-cell immunity against diseases associated with these viruses.

Animals↗
PubMed1995

Parent-to-child transmission is relatively common in the spread of the human polyomavirus JC virus.

JC polyomavirus (JCV), the causative agent of progressive multifocal leukoencephalopathy, is ubiquitous in the human population, infecting children asymptomatically and then persisting in renal tissue. In most adults, renal JCV replicates and the progeny are excreted in urine. We used this urinary JCV to elucidate the routes of JCV transmission. A 610-bp JCV DNA region (IG region) encompassing the 3'-terminal sequences of both T-antigen and VP1 (major capsid protein) genes was amplified by means of PCR from urine specimens collected from all members of seven families. JCV strains were then unequivocally identified by the nucleotide sequences of the amplified IG regions. We could identify 18 distinctive JCV strains from 27 individuals. Different JCV strains were detected from all unrelated persons. However, the same viral strain was detected from one (four families), two (one family), or three offspring (one family) as well as from the fathers (three families) or from the mothers (three families). In total, the JCV strains detected in half of the JCV-positive children were identified in their parents. Since most humans are infected during childhood, these findings indicated that JCV is transmitted frequently from parents to children. We roughly estimated that 50% of JCV transmission occurs by this route and that the other 50% occurs outside the family.

Adult↗
PubMed1998

HIV-1-infected patients with focal neurologic signs: diagnostic role of PCR for Toxoplasma gondii, Epstein-Barr virus, and JC virus.

OBJECTIVE: To evaluate nested PCR for Toxoplasma gondii (TOX), JC virus (JCV) and Epstein-Barr virus (EBV) for diagnosis of toxoplasmic encephalitis (TE), progressive multifocal leukencephalopathy (PML) and primary central nervous system lymphoma (PCL). METHODS: A prospective study encompassed 26 HIV-1-infected individuals presenting with focal neurologic signs and symptoms. Nested PCR was performed on both supernatants and pellets of centrifuged cerebrospinal fluid (CSF), on plasma and on white blood cells (WBCs). For a retrospective study, stored CSF supernatants were available from an additional 27 HIV-1-infected patients with TE, PML, and PCL. RESULTS: TE, PML or PCL was diagnosed in 13 of 26 patients in the prospective group. Plasma and WBC analysis by PCR was not informative except in one case of TE. TOX and JCV were detected by PCR in the CSF pellets of four of five patients with TE, and of four of five patients with PML, respectively, but in no other cases. EBV was detected not only in three of three cases of PCL, but also in six patients suffering from other conditions. PCR on the CSF supernatants was less sensitive for all three etiologies. These results correlated with those of the retrospective PCR analysis, for which only stored CSF supernatants were available, revealing sensitivities of 33%, 50% and 66% for TE, PML and PCL, respectively, but specificities of 100%. CONCLUSIONS: In the clinical routine, TOX and JCV PCR on centrifuged CSF pellets can be recommended to obtain an early diagnosis of TE and PML. Under these conditions, EBV PCR helps to exclude PCL as a cause of FBLs, as it is highly sensitive, but not specific, for PCL in HIV-1-infected individuals.

Journal Article↗
PubMed2003

Lineage pathway of human brain progenitor cells identified by JC virus susceptibility.

Multipotential human central nervous system progenitor cells, isolated from human fetal brain tissue by selective growth conditions, were cultured as undifferentiated, attached cell layers. Selective differentiation yielded highly purified populations of neurons or astrocytes. This report describes the novel use of this cell culture model to study cell type-specific recognition of a human neurotropic virus, JC virus. Infection by either JC virions or a plasmid encoding the JC genome demonstrated susceptibility in astrocytes and, to a lesser degree, progenitor cells, whereas neurons remained nonpermissive. JC virus susceptibility correlated with significantly higher expression of the NFI-X transcription factor in astrocytes than in neurons. Furthermore, transfection of an NFI-X expression vector into progenitor-derived neuronal cells before infection resulted in viral protein production. These results indicate that susceptibility to JC virus infection occurs at the molecular level and also suggest that differential recognition of the viral promoter sequences can predict lineage pathways of multipotential progenitor cells in the human central nervous system.

Brain↗
PubMed1995

[Establishment and analysis of cell culture infected persistently with JC virus].

JC polyomavirus (JCV) is the causative agent of a demyelinating disease in the central nervous system, known as progressive multifocal leukoencephalopathy. Since it is difficult to propagate JCV in vitro, many laboratories have attempted to develop cell lines permissive for replication of JCV. It was recently reported that serial passage of JCV (strain Mad-1) in a human neuroblastoma cell line (IMR-32 cells) generated JCV variants (M1-IMRa, -IMRb, -IMRc) adapted to the growth in IMR-32 cells. We obtained a persistently-infected cell culture, designated JCI cells, by continued subcultivation of IMR-32 cells which had been infected with these adapted variants. To understand the mechanism by which the carrier state was maintained, we molecularly cloned multiple JCV DNAs from JCI cells. Sequencing of the cloned DNAs revealed that a majority of the clones had the same altered regulatory sequence which was probably generated from M1-IMRa. A DNA transfection experiment using a chimeric JCV DNA, in which the regulatory region was derived from JCI and the other region from Mad-1, showed that the JCI regulatory region was less efficient in inducing virus production in IMR-32 cells. Therefore, it could be concluded that the regulatory region is primarily important for maintaining the carrier state in JCI cells. Although JCI cells contained a significant amount of JCV, the yield of JCV could remarkably be increased by incubating a confluent JCI culture in a medium with a low serum concentration. Thus, JCI cells should greatly facilitate the production of JCV for future studies of the virus.

Adolescent↗
PubMed1989

Extension of JC virus host range to monkey cells by insertion of a simian virus 40 enhancer into the JC virus regulatory region.

A chimeric polyomavirus genome was constructed by inserting the 72- and the 21-bp repeats of simian virus 40 (SV40) into the JC virus (JCV) regulatory region on the late side of the JCV 98-bp repeats. Although the chimeric polyomavirus DNA was able to replicate very well in human fetal glial cells, deletions were found in sequences of the regulatory region. DNA sequence analysis of a selected clone indicated a 294-bp deletion from the original construction that retained the sequences for the JCV replication origin, 78 bp of one 98-bp repeat, 33 bp of one SV40 72-bp repeat, and one intact 72-bp repeat. Of significant interest was that this genome demonstrated an extended species and cell-type host range, producing infectious virus in human fetal brain and embryonic kidney as well as in rhesus monkey fetal and adult glial cells. However, the species host range was not extended beyond primate cells since the chimeric polyomavirus was unable to multiply in rodent glial cells. Analysis of the viral RNA transcripts from either kidney or glial cells indicated that the major start sites for early RNA mapped within the JCV sequences of the regulatory region and major start sites for late RNA mapped within the JCV and SV40 sequences. This extension of the JC virus host range was most likely attributable to changes in the regulatory region and not the viral T protein since a recombinant DNA clone which placed the coding sequences for the wild-type JCV T protein subject to regulation by the deleted chimeric regulatory region showed a similar extension of host range.

Animals↗
PubMed1977

Differential neurooncogenicity of strains of JC virus, a human polyoma virus, in newborn Syrian hamsters.

The neurooncogenicity recently isolated strains of the human polyoma virus, JC virus, was determined by intracerebral inoculation of newborn Syrian golden hamsters. All three strains produced malignant brain tumors in a majority of inoculated animals during a 6.5-month observation period. The results obtained with the MAD-2 strain, 19 of 20 animals with cerebellar medulloblastomas and 0 of 20 animals with pineal gland tumors, were quite similar to those observed previously with the prototypic strain of JC virus, MAD-1. Inoculation of the MAD-4 strain, however, resulted in 10 of 22 animals with pineal gland tumors and only 10 of 22 animals with tumors in the cerebellum. The MAD-3 strain was neurooncogenic, but too few animals lived to be weaned to provide significant additional information. The basis for the apparent predilection of the MAD-4 strain for the pineal gland is unknown. Two hamsters in the experiment developed extracranial neuroblastomas.

Abdominal Neoplasms↗
PubMed1992

Evidence that a sequence similar to TAR is important for induction of the JC virus late promoter by human immunodeficiency virus type 1 Tat.

A specific RNA sequence located in the leader of all human immunodeficiency virus type 1 (HIV-1) mRNAs termed the transactivation response element, or TAR, is a primary target for induction of HIV-1 long terminal repeat activity by the HIV-1-derived trans-regulatory protein, Tat. Human neurotropic virus, JC virus (JCV), a causative agent of the degenerative demyelinating disease progressive multifocal leukoencephalopathy, contains sequences in the 5' end of the late RNA species with an extensive homology to HIV-1 TAR. In this study, we examined the possible role of the JCV-derived TAR-homologous sequence in Tat-mediated activation of the JCV late promoter (Tada et al., Proc. Natl. Acad. Sci. USA 87:3479-3483, 1990). Results from site-directed mutagenesis revealed that critical G residues required for the function of HIV-1 TAR that are conserved in the JCV TAR homolog play an important role in Tat activation of the JCV promoter. In addition, in vivo competition studies suggest that shared regulatory components mediate Tat activation of the JCV late and HIV-1 long terminal repeat promoters. Furthermore, we showed that the JCV-derived TAR sequence behaves in the same way as HIV-1 TAR in response to two distinct Tat mutants, one of which that has no ability to bind to HIV-1 TAR and another that lacks transcriptional activity on a responsive promoter. These results suggest that the TAR homolog of the JCV late promoter is responsive to HIV-1 Tat induction and thus may participate in the overall activation of the JCV late promoter mediated by this transactivation.

Base Sequence↗
PubMed2002

Strains of JC virus in Amerind-speakers of North America (Salish) and South America (Guaraní), Na-Dene-speakers of New Mexico (Navajo), and modern Japanese suggest links through an ancestral Asian population.

Previously we showed that strains of human polyoma virus JC among the Navajo in New Mexico, speakers of an Athapaskan language in the Na-Dene language phylum, and among the Salish people in Montana, speakers of a language of the Salishan group in the Amerind family, were mainly of a northeast Asian genotype found in Japan (type 2A). We now report partial VP1-gene, regulatory region, and complete genome sequences of JC virus (JCV) from the Guaraní Indians of Argentina. The Tupí-Guaraní language represents the Equatorial branch of the Amerind language family proposed by Greenberg ([1987] Language in the Americas, Stanford: Stanford University Press). The partial VP1 gene sequences of the Guaraní revealed several variants of strains found in northeast Asia (Japan), as did the Salish. In contrast, the strains in the Navajo largely conformed to the prototype type 2A sequence (MY). Phylogenetic reconstruction with both the neighbor-joining and maximum parsimony methods utilized three complete Guaraní JCV genome sequences, three genomes from the Salish people, and 27 other complete JCV genomes, including three from the Navajo and three from Japan. Both trees showed that all type 2A JCV strains from the North and South Americans are closely related phylogenetically to strains in present-day Japan. However, variant sites in the coding regions, the T-antigen intron, and the regulatory region link the type 2A strains in Amerind groups (Guaraní and Salish), but differentiate them from those in a Na-Dene-speaking (Navajo) population. The data suggest separation from a population ancestral to modern Japanese, followed by a second division within the ancestral group that led to Amerind- and Na-Dene-speaking groups. The data cannot, however, localize the latter split to the Asian mainland (two migrations) or to North America (one migration).

Adult↗
PubMed2001

Increased frequency of JC virus type 2 and of dual infection with JC virus type 1 and 2 in Italian progressive multifocal leukoencephalopathy patients.

To verify the possibility of different role of JC virus genotypes in the etiology of progressive multifocal leukoencephalopathy, we analysed several JC virus isolates amplified from AIDS patients with and without progressive multifocal leukoencephalopathy and healthy controls by nucleotide sequencing. Cerebrospinal fluid (CSF), peripheral blood mononuclear cells (PBMCs) and urine from 52 AIDS patients suffering from various neurological diseases including 21 cases of progressive multifocal leukoencephalopathy, and PBMCs and urine from healthy subjects were evaluated by nested polymerase chain reaction (PCR) for the presence of DNA belonging to the highly conserved large T antigen (LT) of JC virus. The different JC virus subtypes were identified by nucleotide sequence analysis of the virion protein (VP1) genomic region. JC virus DNA was detected in all the CSF samples from the progressive multifocal leukoencephalopathy patients, but not in the CSF from non-progressive multifocal leukoencephalopathy cases, while the frequency of JC virus DNA detection in the PBMCs and urine did not differ among the three groups studied. JC virus type 2 was detected only in progressive multifocal leukoencephalopathy patients, and in particular in 52.4% of their CSF samples. Moreover, in the CSF of 19.0% of the progressive multifocal leukoencephalopathy cases, dual infection with both JC virus types 1 and 2 was found. The data obtained in this study indicate that the unexpected involvement of JC virus type 2, a strain not common in Italy, and the high frequency of dual infection with both JC virus types 1 and 2 in progressive multifocal leukoencephalopathy CSF, can be indications of risk factors for progressive multifocal leukoencephalopathy development.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Human immunodeficiency virus (HIV) and JC virus in acquired immune deficiency syndrome (AIDS) patients with progressive multifocal leukoencephalopathy.

Of the 93 acquired immune deficiency syndrome (AIDS) patients autopsied between 1983 and 1986, 27 had evidence of viral encephalitis of which 3 had progressive multifocal leukoencephalopathy (PML), confirmed by electron microscopy. Using in situ hybridization with biotinylated JC virus probes, paraffin sections from the brains of these 27 patients were examined. JC virus was found only in those patients with histologically proven PML, while no evidence of JC virus was detected in the brains of the other 24 AIDS patients despite the presence of white matter pathology. Brain biopsies of the PML patients demonstrated human immunodeficiency virus (HIV)-infected macrophages infiltrating regions of demyelination. When the patients died (2 to 6 months after diagnosis of PML), many more macrophages contained HIV antigens and some had fused to form multinucleated giant cells. These findings suggest that in AIDS patients, papovaviruses not only cause damage by directly infecting oligodendroglia but causes additional damage by eliciting the ingress of macrophages latently infected with HIV. As was seen with other infections (e.g., cytomegalovirus) of the CNS this might be a general mechanism of HIV entry into the brain.

Acquired Immunodeficiency Syndrome↗
PubMed1979

Perinatal induction of medulloblastomas in Syrian golden hamsters by a human polyoma virus (JC).

Medulloblastomas, originating from cells of the internal granular layer of the cerebellum, developed in Syrian golden hamsters 3--6 months after inoculation at birth intracerebrally and sc with JC virus, a papovavirus isolated originally from a human case of the demyelinating disease progressive multifocal leukoencephalopathy. The lesion is compared with the human medulloblastoma of childhood. JC virus is the first infectious agent to produce such a neoplasm in any species.

Animals↗
PubMed1994

A 70- to 80-kDa glial cell protein interacts with the AGGGAAGGGA domain of the JC virus early promoter only in the presence of the neighboring cis DNA elements.

The neurotropic virus JC (JCV) causes the demyelinating disease progressive multifocal leukoencephalopathy. JCV is transcriptionally regulated by both positive and negative cis elements. Previous studies have shown that the AGGGAAGGGA sequence, in isolation, interacts with a 53- to 56-kDa cellular protein and acts as a silencer for the late promoter. We have reexamined the role of the AGGGAAGGGA element in the glial cell-specific transcriptional regulation of JCV by studying it in a longer natural context of elements of the JCV early promoter. Transcriptional analysis in C6 glial cells of selectively mutated AGGGAAGGGA domains within the nt 98-153 region of the JCV early promoter revealed that both GGG regions in the AGGGAAGGGA sequence are required for glial cell-specific transcription. The interactions of cellular proteins with the AGGGAAGGGA domain were also found to be dependent upon the presence or absence of neighboring cis elements. The TATA region was found to facilitate the interaction of specific proteins with the AGGGAAGGGA domain. Domain-specific photocrosslinking studies revealed the binding of a glial cell protein of approximately 70-80 kDa to the AGGGAAAGGGA domain only when it was flanked by its neighboring cis elements, the TATA and NF-1 domains of the JCV promoter.

Affinity Labels↗
PubMed1999

Human anti-JC virus serum reacts with native but not denatured JC virus major capsid protein VP1.

The immunoreactivity of human anti-JC virus (JCV) serum against the major capsid protein VP1 of JCV was analyzed by Western blot, dot blot, and hemagglutination inhibition (HAI) assays. JCV-positive human serum reacted with native but not denatured JCV major capsid protein VP1, as demonstrated by dot blot and Western blot. Rabbit antiserum raised against native JCV capsid had immunoreactivities similar to those of human anti-JCV serum. These results indicate that the antigenecity of native and denatured JCV VP1 is different. In addition, both JCV-positive human serum and rabbit antiserum raised against native JCV capsid protein inhibited the hemagglutination activity of JCV capsid particles. In contrast, rabbit antiserum raised against denatured JCV VP1 did not inhibit hemagglutination. These findings reveal that denaturation may alter the antigenic epitopes of JCV VP1. Therefore, keeping the JCV capsid protein native appears to be essential for serological or other immunological analyses of the virus.

Animals↗