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Chronic infections of the human immunodeficiency virus (HIV) create a verycomplex co-evolutionary process, where the virus tries to escape thecontinuously adapting host immune system. Quantitative details of this processare largely unknown and could help in disease treatment and vaccinedevelopment. Here we study a longitudinal dataset of ten HIV-infected people,where both the B-cell receptors and the virus are deeply sequenced. We focus onsimple measures of turnover, which quantify how much the composition of theviral strains and the immune repertoire change between time points. At thesingle-patient level, the viral-host turnover rates do not show anystatistically significant correlation, however they correlate if theinformation is aggregated across patients. In particular, we identify ananti-correlation: large changes in the viral pool composition come with smallchanges in the B-cell receptor repertoire. This result seems to contradict thenaive expectation that when the virus mutates quickly, the immune repertoireneeds to change to keep up. However, we show that the observed anti-correlationnaturally emerges and can be understood in terms of simple population-geneticsmodels.

Inspecting the interaction between HIV and the immune system through genetic turnover