作者: Christiaan H. van Dorp , Michiel van Boven , Rob J. de Boer
DOI: 10.1371/JOURNAL.PCBI.1003899
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摘要: It has been suggested that HIV-1 evolved its set-point virus load to be optimized for transmission. Previous epidemiological models and studies into the heritability of confirm this mode adaptation within human population is feasible. However, during many cycles replication between infection a host transmission next host, under selection escape from immune responses, not Here we investigate with computational mathematical how these two levels selection, within-host between-host, are intertwined. We find when rate comparable what observed in patients, hosts dominant over Surprisingly, do high values heritability, argue estimates can caused by ‘footprints’ left differing hosts' systems on virus.