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J. Virol., Dec 1995, 7606-7611, Vol 69, No. 12
N Watanabe, T Yugawa, Y Ikawa and H Amanuma
Friend spleen focus-forming virus (F-SFFV) causes acute erythroleukemia in
mice and encodes in its defective env gene an Env-like membrane
glycoprotein (gp55). The F-SFFV env gene has three characteristic
structures compared with that of ecotropic murine leukemia viruses (MuLVs):
substitution by the polytropic MuLV env sequence, a 585-bp deletion, and a
1-bp insertion. All of these characteristic structures are essential for
the leukemogenic potential of gp55 of polycythemia- inducing isolates of
F-SFFV (F-SFFVp). The 1-bp insertion causes changes of six amino acids and
truncation by 34 amino acids at the C terminus. In this study, we
constructed 12 mutant F-SFFV genomes starting from the wild-type F-SFFVp
and examined the effect of the C- terminal truncation and the six altered
amino acids on the pathogenic activity of gp55. The results indicated that
at least 18 to 24 amino acids must be deleted from the C terminus for the
env product to be pathogenically active. We also found that the six altered
amino acids contributed significantly to the pathogenic activity of gp55.
Analyses of the cellular processing of these mutant gp55s supported a
correlation between the pathogenic activity of gp55 and its efficiency in
overall cellular processing.
Copyright © 1995, American Society for Microbiology
Both the changes of six amino acids and the C-terminal truncation caused by a one-base insertion in the defective env gene of Friend spleen focus-forming virus significantly affect the pathogenic activity of the encoded leukemogenic membrane glycoprotein (gp55)
Laboratory of Gene Technology and Safety, Tsukuba Life Science Center, Institute of Physical and Chemical Research (RIKEN), Ibaraki, Japan.
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