J. Virol., 10 1997, 7145-7156, Vol 71, No. 10
K Kizhatil and LM Albritton
Murine ecotropic leukemia viruses use a common receptor for entry into host
cells; however, the site of virus fusion appears to differ with the host
cell. Entry in mouse NIH 3T3 fibroblasts is by endocytosis, whereas entry
in rat XC sarcoma cells is by surface fusion. We report here the
identification of a step common to both entry pathways, as well as of a
step unique to the endocytic pathway. Recent demonstration of the
clustering of the virus receptor on rat cells suggested a possible
interaction of the receptor with the cellular cytoskeleton (M. H. Woodard,
W. A. Dunn, R. O. Laine, M. Malandro, R. McMahon, O. Simell, E. R. Block,
and M. S. Kilberg, Am. J. Physiol. 266:E817-E824, 1994). We tested the
hypothesis that such an interaction might influence receptor function. We
found that entry into NIH 3T3 and XC cells was greatly diminished by the
disruption of the actin network before but not shortly after virus
internalization, suggesting the actin network plays a critical role in an
early step common to both entry pathways. Disruption of microtubules before
and shortly after virus internalization markedly reduced entry in NIH 3T3
cells, while entry into XC cells remained efficient. These data suggest
that intact microtubules are required in a postpenetration step unique to
efficient virus entry via endocytosis. The physiological function of the
receptor was not affected by disruption of either the actin network or the
microtubules, as the uptake of cationic amino acids in NIH 3T3 and XC cells
was comparable to that in control cells even when the cytoskeleton remained
disrupted for as long as 3 h.
Copyright © 1997, American Society for Microbiology
Requirements for different components of the host cell cytoskeleton distinguish ecotropic murine leukemia virus entry via endocytosis from entry via surface fusion
Department of Microbiology and Immunology, College of Medicine, University of Tennessee-Memphis, 38163, USA.
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