  Viral infection requires the binding of receptors on the target cell membrane
to glycoproteins, or ``spikes,'' on the viral membrane. The initial entry is
usually classified as fusogenic or endocytotic. However, binding of viral
spikes to cell surface receptors not only initiates the viral adhesion and the
wrapping process necessary for internalization, but can simultaneously initiate
direct fusion with the cell membrane. Both fusion and internalization have been
observed to be viable pathways for many viruses. We develop a stochastic model
for viral entry that incorporates a competition between receptor mediated
fusion and endocytosis. The relative probabilities of fusion and endocytosis of
a virus particle initially nonspecifically adsorbed on the host cell membrane
are computed as functions of receptor concentration, binding strength, and
number of spikes. We find different parameter regimes where the entry pathway
probabilities can be analytically expressed. Experimental tests of our
mechanistic hypotheses are proposed and discussed.
