Abstract
Set point viral load in HIV patients ranges over several orders of magnitude and is a key determinant of disease progression in HIV. A number of recent studies have reported high heritability of set point viral load implying that viral genetic factors contribute substantially to the overall variation in viral load. The high heritability is surprising given the diversity of host factors associated with controlling viral infection. Here we develop an analytical model that describes the temporal changes of the distribution of set point viral load as a function of heritability. This model shows that high heritability is the most parsimonious explanation for the observed variance of set point viral load. Our results thus not only reinforce the credibility of previous estimates of heritability but also shed new light onto mechanisms of viral pathogenesis.
Highlights
The time course of viral load in HIV infected patients follows a characteristic pattern
Following an initial peak in viremia, the viral load in HIV infected patients settles down to a set point which remains more or less stable during chronic HIV infection. This set point viral load is one of the key factors determining the rate of disease progression
The extent to which it is determined by the virus versus host genetics is central to developing a better understanding of disease progression
Summary
The time course of viral load in HIV infected patients follows a characteristic pattern. During primary infection the viral load rapidly grows to very high levels. The peak viremia is attained within the first few weeks of infection. Thereafter the viral load declines rapidly over a period of several months and eventually settles down at a much lower level referred to as the viral set point. Set point viral load (spVL) is a central characteristic of the course of the disease. The virus load measurements do fluctuate in patients, the time average of the viral load remains remarkably close to the spVL in most of patients over the time scale of several years [1, 2]. Higher spVL is associated with faster disease progression [3]
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