Persistence of neurotropic JC virus DNA in hamster tissues six months after intracerebral inoculation.
Journal - Journal of neurovirology (ENGLAND )
Immunostaining and polymerase chain reaction (PCR) methods were used to examine tissues from 18 6-month-old hamsters intracerebrally inoculated with JC virus (JCV) as newborns. JCV DNA was detected in all hamster brains and urinary bladders, as well as in most kidney, adrenal gland and pancreas samples. While results from reverse transcription PCR (RNA PCR) and immunostaining suggest that T antigen transcription and protein expression were restricted to the brain, the DNA suggests that intracerebrally inoculated JCV enters the systemic circulation and latently infects organs in a tissue specific manner.
|ISSN : ||1355-0284|
|Mesh Heading : ||Adrenal Gland Neoplasms Animals Brain Cricetinae DNA, Viral Female Gonads Injections JC Virus Male Mesocricetus Neuroblastoma Papillomavirus Infections Time Factors Tissue Distribution Tumor Virus Infections Viscera virology virology analysis virology isolation & purification virology virology|
|Mesh Heading Relevant : ||physiology virology virology virology|
Brain vascular endothelial cells express JC virus large tumor antigen in immunocompetent and cyclophosphamide-treated hamsters.
Journal - Proceedings of the National Academy of Sciences of the United States of America (UNITED STATES )
When injected intracerebrally into newborn hamsters, the human polyomavirus JC virus (JCV) establishes a nonproductive infection resulting in brain tumor formation. Using immunostaining methods to detect the JCV regulatory protein, large tumor antigen (T antigen), we have now demonstrated JCV infection of brain vascular endothelial cells (EC) in infected hamsters. JCV T antigen was detected in lectin-labeled EC as well as in von Willebrand factor-expressing EC in both cyclophosphamide-treated and nonimmunosuppressed hamster brains 16, 21, and 31 days after birth. Cyclophosphamide-treated hamsters exhibited a greater number of JCV-infected EC, whereas T-antigen expression in nonvascular cells was not affected. The influence of cyclophosphamide was most pronounced in the cerebellum where increased numbers of JCV-infected EC were located predominantly at the internal granular layer-white matter junction, also a prominent location for T-antigen-expressing neoplastic foci. The hamster model demonstrates in vivo infection of EC by a human polyomavirus and directs interest toward the role of these cells in human JCV infection.
|ISSN : ||0027-8424|
|Mesh Heading : ||Animals Antigens, Polyomavirus Transforming Blood-Brain Barrier Cerebellum Cricetinae Cyclophosphamide Endothelium, Vascular Immunoenzyme Techniques JC Virus Mesocricetus Tumor Virus Infections von Willebrand Factor microbiology immunology metabolism|
|Mesh Heading Relevant : ||metabolism microbiology immunology immunology|
Immunolabeling of JC virus large T antigen in neonatal hamster brain before tumor formation.
Journal - Laboratory investigation; a journal of technical methods and pathology (UNITED STATES )
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. Three days after intracerebral inoculation of 2500 hemagglutinating units of JCV, T antigen was expressed predominantly in nuclei of cells in the external granular layer and newly forming internal granular layer of the cerebellum and also in cell nuclei located in the hippocampus, periventricular areas, and the olfactory bulb. At 7 days postinoculation (p.i.), most cerebellar T antigen-containing cells had migrated to the internal granular layer, but by 15 days p.i., cells that expressed T antigen was greatly reduced in number or absent. However, by 30 days p.i., the internal granular layer of the cerebellum again contained T antigen-positive cells. In contrast to the scattered cells seen at 3 or 7 days p.i., these cells appeared in dense clusters thought to represent pretumor foci. Since JCV capsid proteins were not detected at any time, JCV may establish a latent or abortive infection in cells during their mitotic phase and these cells initially express T-antigen during migration or become immunoreactive later before tumor formation.
|ISSN : ||0023-6837|
|Mesh Heading : ||Animals Animals, Newborn Antigens, Viral Brain Brain Neoplasms Capsid Cricetinae Immunologic Techniques Injections JC Virus Polyomavirus Staining and Labeling Time Factors Tissue Distribution metabolism metabolism physiology|
|Mesh Heading Relevant : ||analysis immunology etiology immunology immunology|