  The canonical view of the interactions between viruses and their microbial
hosts presumes that changes in host and virus fate require the initiation of
infection of a host by a virus. That is, first virus particles diffuse randomly
outside of host cells, then the virus genome enters the target host cell, and
only then do intracellular dynamics and regulation of virus and host cell fate
unfold. Intracellular dynamics may lead to the death of the host cell and
release of viruses, to the elimination of the virus genome through cellular
defense mechanisms, or the integration of the virus genome with the host as a
chromosomal or extra-chromosomal element. Here we revisit this canonical view,
inspired by recent experimental findings of Bautista and colleagues (mBio,
2015) in which the majority of target host cells can be induced into a dormant
state when exposed to either active or de-activated viruses, even when viruses
are present at low relative titer. We propose that both the qualitative
phenomena and the quantitative time-scales of dormancy induction can be
reconciled given the hypothesis that cellular physiology can be altered by
contact on the surface of host cells rather than strictly by infection. We
develop a biophysical model of contact-mediated dynamics involving virus
particles and target cells. We show how in this model virus particles can
catalyze - extracellularly - cellular transformations amongst many cells, even
if they ultimately infect only one (or none). We discuss implications of the
present biophysical model relevant to the study of virus-microbe interactions
more generally.
