Soumya B
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 (τ1) would lead to a concomitant increase in peak viremia. However increasing this time would also invite a more vigorous response from Cytotoxic TLymphocytes (CTLs). Simultaneously, if there is a vigorous antibody response, then we might expect τ1 to be high, in order that the virus builds up its population and conversely if there is a weak antibody response, τ1 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.
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