Viral reproductive strategies: How can lytic viruses be evolutionarily competitive?
Viral release strategies can be roughly classified as lytic (the ones that accumulate inside the host cell and exit in a burst, killing the cell), and budding (the ones that are produced and released from the host cell gradually). Here we study the evolutionary competition between the two strategies. If all the parameters, such as the rate of viral production, cell life-span and the neutralizing capacity of the antibodies, were the same for lytic and budding viruses, the budding life-strategy would have a large evolutionary advantage. The question arises what makes lytic viruses evolutionarily competitive. We propose that it is the different removal capacity of the antibodies against budding and lytic virions. The latter exit the cell in a large burst such that the antibodies are "flooded" and a larger proportion of virions can escape the immune system and spread to new cells. We create two spatial models of virus-antibody interaction and show that for realistic parameter values, the effect of antibody flooding can indeed take place. We also argue that the lytic life cycle, including a relatively large burst-size, has evolved to promote survival in the face of antibody attack. According to the calculations, in the absence of efficient antibodies, the optimal burst size of lytic viruses would be only a few virus particles, as opposed to the observed 10(2)-10(5) viral particles. Similarly, there is an evolutionary pressure to extend the life-span as a response to antibody action.
Komarova
Natalia L
NL
Department of Mathematics, University of California, Irvine, CA 92697, USA. komarova@math.uci.edu
D000818:Animals; D000914:Antibodies, Viral / Q000276:immunology; D005075:Biological Evolution; D003588:Cytopathogenic Effect, Viral; D054884:Host-Pathogen Interactions / Q000276:immunology*; D008954:Models, Biological; D018448:Models, Immunological; D014771:Virion / Q000502:physiology; D014774:Virulence; D014777:Virus Diseases / Q000276:immunology* / Q000821:virology; D014779:Virus Replication; D014780:Viruses / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*
D000914:Antibodies, Viral