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Journal of Virology, September 2000, p. 8757-8761, Vol. 74, No. 18
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Is the 135S Poliovirus Particle an Intermediate during Cell
Entry?
Yan
Huang,1
James
M.
Hogle,2 and
Marie
Chow1,*
Department of Microbiology and Immunology, University of
Arkansas for Medical Sciences, Little Rock, Arkansas
72205,1 and Department of Biological
Chemistry and Molecular Pharmacology, Harvard Medical School, Boston,
Massachusetts 021152
Received 18 January 2000/Accepted 20 June 2000
Poliovirus binding to its receptor (PVR) on the cell surface
induces a conformational transition which generates an altered particle
with a sedimentation value of 135S versus the 160S of the native
virion. A number of lines of evidence suggest that the 135S particle is
a cell entry intermediate. However, the low infection efficiencies of
the 135S particle and the absence of detectable 135S particles during
infection at 26°C by the cold-adapted mutants argue against a role
for the 135S particle during the cell entry process. We show here that
binding of 135S-antibody complexes to the Fc receptor (CDw32) increases
the infectivity of these particles by 2 to 3 orders of magnitude. Thus,
the low efficiency of infection by 135S particles is due in part to the low binding affinity of these particles. In addition, we show that
there is an additional stage in the entry process that is associated
with RNA release. This stage occurs after formation of the 135S
particle, is rate limiting during infection at 37°C, but not at
26°C, and is PVR independent. The data also demonstrate that during
infection at 26°C, the rate-limiting step is the PVR-mediated conversion of wild-type 160S particles to 135S particles. This suggests
that during infection at 26°C by the cold-adapted viruses, 135S
particles are formed, but they fail to accumulate to detectable levels
because the subsequent post-135S particle events occur at a
significantly faster rate than the initial conversion of 160S to 135S
particles. These data support a model in which the 135S particle is an
intermediate during poliovirus entry.
*
Corresponding author. Mailing address: University of
Arkansas for Medical Sciences, 4301 W. Markham, Slot 511, Little Rock, AR 72205. Phone: (501) 686-5155. Fax: (501) 686-5362.
Journal of Virology, September 2000, p. 8757-8761, Vol. 74, No. 18
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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