Disease relevance of gp64

• Baculovirus gp64 gene expression: negative regulation by a minicistron [1].
• Immunocytochemical analysis showed that BmNPV was not imported into the nucleus of these two cell lines, while recombinant BmNPV, vBmDelta64/ac-gp64 possessing AcMNPV gp64 was imported into the nucleus, yielding progeny virions in High Five cells, but not Sf9 cells [2].
• Transcripts for the gp64 and polyhedrin genes as well as a 1629 open reading frame (1629 ORF) of the Autographa californica nuclear polyhedrosis virus were examined in the midgut tissues and hemocytes of uninfected and infected host Trichoplusia ni larvae and Sf21 cells [3].

High impact information on gp64

• In subsequent experiments, a cat reporter was fused in frame to the downstream gp64 ORF, and various constructs containing point mutations that inactivated the minicistron were examined [1].
• These results indicate that the defective nuclear import of infected virions due to insufficient BmNPV GP64 function is involved in the restricted BmNPV replication in Sf9 and High Five cells [2].
• Our results showed that insertion of the RGD-peptide into the envelope protein gp64 leads to enhanced specific uptake of baculoviral particles in mammalian cells, only when a combination of wild-type and mutant gp64 was present on the viral surface [4].

Analytical, diagnostic and therapeutic context of gp64

• Specific binding of the gp64 fusion viruses to mammalian target cells was demonstrated by using monoclonal anti-gp64 antibodies followed by fluorescence and/or confocal microscopy [5].

References