The ability of murine polyomavirus (MPyV)-VP1 virus-like particles (MPyV-VLPs) to immunize against MPyV tumour outgrowth was investigated. Non-immunized and mice immunized three times were challenged with MPyV or non-MPyV tumours and followed for tumour outgrowth. MPyV-VLP immunization abrogated outgrowth of some, but not all, tested MPyV tumours and delayed the outgrowth of a non-MPyV tumour to some extent.
View Article and Find Full Text PDFIn two tumour sublines (T.wt/BL and T.wt/Bc), established from mammary adenocarcinomas caused by mouse polyoma (Py) infection of nu/nu mice, integration of polyomavirus DNA sequences into the c-myc gene locus was mapped.
View Article and Find Full Text PDFThe ability to vaccinate against polyomavirus infection in a T-cell deficient as well as a normal immune context was studied using polyomavirus major capsid protein (VP1) pseudocapsids (VP1-ps) or a glutathione-S-transferase-VP1 (GST-VP1) fusion protein. VP1-ps (1 or 10 microg) were administered subcutaneously, alone or together with Freund's complete and incomplete adjuvant, to CD4(-/-)8(-/-) T-cell deficient or normal C57Bl/6 mice on four occasions. Alternatively, CD4(-/-)8(-/-) and normal mice were inoculated with either GST-VP1 or Py-VP1-ps (5 microg).
View Article and Find Full Text PDFPolyomavirus reaches the nucleus in a still encapsidated form, and the viral genome is readily found in association with the nuclear matrix. This association is thought to be essential for viral replication. In order to identify the protein(s) involved in the virus-nuclear matrix interaction, we focused on the possible roles exerted by the multifunctional cellular nuclear matrix protein Yin Yang 1 (YY1) and by the viral major capsid protein VP1.
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