Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-4-15
pubmed:abstractText
The 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). Following immunisation, antibody titres were tested by ELISA to VP1-ps or GST-VP1 or by haemagglutination inhibition (HAI). Mice were then infected with polyomavirus. Three weeks post-infection, the mice were killed and examined for the presence of polyomavirus DNA by PCR. Viral DNA was not detected in CD4(-/-)8(-/-) mice immunised with either VP1-ps alone or in combination with Freund's complete and incomplete adjuvant, or in any of the normal mice immunised with VP1-ps or GST-VP1. However, viral DNA was detected in 2/5 of the CD4(-/-)8(-/-) mice immunised with GST-VP1 and in non-immunised controls. Greater antibody titres were observed to VP1-ps than to GST-VP1 in CD4(-/-)8(-/-) mice after VP1-ps compared to GST-VP1 immunisation and antibody responses were better in normal than in immune-deficient mice. Only immunisation with VP1-ps resulted in haemagglutination inhibition. Complete protection against polyomavirus infection in the T-cell deficient context was obtained with VP1-ps, but not with GST-VP1, immunisation using the present vaccination protocol.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0146-6615
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
293-300
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12696121-Animals, pubmed-meshheading:12696121-Antibodies, Viral, pubmed-meshheading:12696121-Capsid, pubmed-meshheading:12696121-Capsid Proteins, pubmed-meshheading:12696121-Disease Models, Animal, pubmed-meshheading:12696121-Glutathione Transferase, pubmed-meshheading:12696121-Guinea Pigs, pubmed-meshheading:12696121-Hemagglutination, pubmed-meshheading:12696121-Humans, pubmed-meshheading:12696121-Immunization, pubmed-meshheading:12696121-Immunologic Deficiency Syndromes, pubmed-meshheading:12696121-Mice, pubmed-meshheading:12696121-Mice, Inbred C57BL, pubmed-meshheading:12696121-Polyomavirus, pubmed-meshheading:12696121-Polyomavirus Infections, pubmed-meshheading:12696121-Recombinant Fusion Proteins, pubmed-meshheading:12696121-T-Lymphocytes, pubmed-meshheading:12696121-Tumor Virus Infections, pubmed-meshheading:12696121-Viral Vaccines
pubmed:year
2003
pubmed:articleTitle
VP1 pseudocapsids, but not a glutathione-S-transferase VP1 fusion protein, prevent polyomavirus infection in a T-cell immune deficient experimental mouse model.
pubmed:affiliation
Department of Oncology-Pathology, Karolinska Institute, Karolinska Hospital, SE-171 76 Stockholm, Sweden. Andrea.Vlastos@cck.ki.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't