Human herpesvirus-6 infection may predispose cells to superinfection by other viruses.
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.
Schonnebeck
M
M
Immunopathology Laboratory, University of Cologne, Germany.
Krueger
G R
GR
Braun
M
M
Fischer
M
M
Koch
B
B
Ablashi
D V
DV
Balachandran
N
N
D002460:Cell Line; D002470:Cell Survival; D002472:Cell Transformation, Viral; D002788:Cholesterol Esters / Q000494:pharmacology; D015342:DNA Probes; D004279:DNA, Viral / Q000302:isolation & purification; D015497:HIV-1 / Q000235:genetics*; D004854:Herpesvirus 4, Human / Q000235:genetics*; D015654:Herpesvirus 6, Human / Q000235:genetics*; D006801:Humans; D007700:Kinetics; D008560:Membrane Fluidity / Q000187:drug effects; D009693:Nucleic Acid Hybridization
D002788:Cholesterol Esters; D015342:DNA Probes; D004279:DNA, Viral; C013440:cholesteryl succinate