Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1991-10-23
pubmed:abstractText
Double infection of cells by HHV-6, Epstein-Barr virus (EBV) and by human immunodeficiency virus (HIV-1) can enhance viral effects though genetic transactivation. It remained to be clarified, however, by which mechanism different viruses may enter the same cell. We have shown that HHV-6 infection of immature lymphoid cells rigidifies the cytoplasmic membrane and causes receptor proteins for viruses such as CD4 for HIV-1 and CR2 for EBV to be expressed. In our experiments, HHV-6 infected cells were superinfected by HIV1 and caused enhanced cell death. The mechanisms by which receptors were expressed after HHV-6 infection appears independent of cell membrane rigidification alone and is suppressed by cycloheximide only to a certain extent.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0258-851X
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
255-63
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
Human herpesvirus-6 infection may predispose cells to superinfection by other viruses.
pubmed:affiliation
Immunopathology Laboratory, University of Cologne, Germany.
pubmed:publicationType
Journal Article