The molecular mechanism of cell entry by unenveloped viruses is poorly
understood. The picornaviruses poliovirus, human rhinovirus, and coxs
ackievirus convert to an altered form (the 135S or A particle) upon in
teraction with receptors on susceptible Cells at 37 degrees C, The 135
5 particle is thought to be a necessary intermediate because it accumu
lates inside susceptible cells soon after infection and drugs which in
hibit conversion of the virus to this form also prevent infection, How
ever, since a variable fraction of the altered 135S particles is repor
ted to elute unproductively hom the surface of susceptible cells, thei
r precise role remains unclear, We have found that poliovirus 135S par
ticles can infect Chinese hamster ovary (CHO) and murine L cells, neit
her of which are susceptible to infection by native poliovirus. The in
fectivity of the particles in tissue culture appears to be between 10(
3) to 10(5) times less than that of poliovirus on HeLa cells, The 135S
particle infectivity was not sensitive to RNase but was greatly reduc
ed by proteolytic treatment, Proteolysis specifically removed the newl
y exposed N terminus of VP1, a feature which has previously been shown
to mediate interactions of the particle with lipid membranes, These r
esults demonstrate that although the infectivity of the 135S particle
appears to be receptor independent, it nonetheless requires some prope
rty associated with the protein coat. In particular, the N terminus of
VP1 plays an important role in the infection process, Our findings ar
e consistent with the hypothesis that the 135S particle is an intermed
iate in the normal cell entry pathway of poliovirus infection.