Bound simian virus 40 translocates to caveolin-enriched membrane domains, and its entry is inhibited by drugs that selectively disrupt caveolae.
HA Anderson, Y Chen, LC Norkin - Molecular biology of the cell, 1996 - Am Soc Cell Biol
HA Anderson, Y Chen, LC Norkin
Molecular biology of the cell, 1996•Am Soc Cell BiolSimian virus 40 (SV40) entry leading to infection occurred only after the virus was at the cell
surface for 1.5 to 2 h. SV40 infectious entry was not sensitive to cytosol acidification, a
treatment that blocks endocytosis via clathrin-coated vesicles. Instead, SV40 infectious entry
was blocked by treating cells with the phorbol ester PMA or nystatin, which selectively
disrupts caveolae. In control experiments, transferrin internalization was sensitive to cytosol
acidification but was not sensitive to PMA or nystatin. Also, absorbed transferrin entered …
surface for 1.5 to 2 h. SV40 infectious entry was not sensitive to cytosol acidification, a
treatment that blocks endocytosis via clathrin-coated vesicles. Instead, SV40 infectious entry
was blocked by treating cells with the phorbol ester PMA or nystatin, which selectively
disrupts caveolae. In control experiments, transferrin internalization was sensitive to cytosol
acidification but was not sensitive to PMA or nystatin. Also, absorbed transferrin entered …
Simian virus 40 (SV40) entry leading to infection occurred only after the virus was at the cell surface for 1.5 to 2 h. SV40 infectious entry was not sensitive to cytosol acidification, a treatment that blocks endocytosis via clathrin-coated vesicles. Instead, SV40 infectious entry was blocked by treating cells with the phorbol ester PMA or nystatin, which selectively disrupts caveolae. In control experiments, transferrin internalization was sensitive to cytosol acidification but was not sensitive to PMA or nystatin. Also, absorbed transferrin entered cells within minutes. Finally, bound SV40 translocated to caveolin-enriched membrane complexes isolated by a Triton X-100 insolubility protocol. Treatment with nystatin did not impair SV40 binding but did block the partitioning of virus into the caveolin-enriched complexes.
Am Soc Cell Biol