  This paper explores a number of questions regarding optimal strategies
evolved by viruses upon entry into a vertebrate host. The infected cell life
cycle consists of a non-productively infected stage in which it is producing
virions but not releasing them and of a productively infected stage in which it
is just releasing virions. The study explores why the infected cell cycle
should be so delineated, something which is akin to a classic bang-bang control
or all-or-none principle. The times spent in each of these stages represent a
viral strategy to optimize peak viral load. Increasing the time spent in the
non-productively infected phase ({\tau}1) would lead to a concomitant increase
in peak viremia. However increasing this time would also invite a more vigorous
response from Cytotoxic T-Lymphocytes (CTLs). Simultaneously, if there is a
vigorous antibody response, then we might expect {\tau}1 to be high, in order
that the virus builds up its population and conversely if there is a weak
antibody response, {\tau}1 might be small. These tradeoffs are explored using a
mathematical model of virus propagation using Ordinary Differential Equations
(ODEs). The study raises questions about whether common viruses have actually
settled into an optimum, the role for reliability and whether experimental
infections of hosts with non-endemic strains could help elicit answers about
viral progression.
