科研之友
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摘要
With non-adherence operationally defined as a sharp increase in viral load in the absence of mutation, it is hypothesised that periods of non-adherence can be identified retrospectively based on the observed relationship between changes in viral load and mutation.Spikes in the viral load (VL) can be identified from time periods over which VL rises above the undetectable level to a point at which the VL decreases by a threshold amount. The presence of mutations can be established by comparing each sequence to a reference sequence and by comparing sequences in pairs taken sequentially in time, in order to identify changes within the sequences at or around 'treatment change events'. Observed spikes in VL measurements without mutation in the corresponding sequence data then serve as a proxy indicator of non-adherence.It is envisaged that the validation of the hypothesised approach will serve as a first step on the road to clinical practice. The information inferred from clinical data on adherence would be a crucially important feature of treatment prediction tools provided for practitioners to aid daily practice. In addition, distinct characteristics of biological markers routinely used to assess the state of the disease may be identified in the adherent and non-adherent groups. This latter approach would directly help clinicians to differentiate between non-responding and non-adherent patients.Whilst the first cases of AIDS were identified in the USA [1,2], and shortly after in Europe [3,4] it is now known that the disease originated from sub-Saharan Africa [5], which currently holds two thirds of the world's 33.2 million people living with HIV. Recent estimates also suggest that Africa has 1.7 million of the global 2.5 million individuals newly infected during 2007 [6]. During 1983, 3,064 people in the US were found to have AIDS, of which a third died [7]; the number infected had risen to 20,745 by 1987 [8]. The rapid spread of HIV over the early pre-treatment years i
- 出版日期2009
