Despite three decades of research, an HIV vaccine remains elusive. The main reason for this is the virus’s uncanny ability to evolve resistance to immune control, so understanding how the virus adapts to the earliest immune responses is critical for success. Recent
Despite three decades of research, an HIV vaccine remains elusive. The main reason for this is the virus’s uncanny ability to evolve resistance to immune control, so understanding how the virus adapts to the earliest immune responses is critical for success. Recent work involving computer simulation provides some insight into the problem we face.
Most infections by human immunodeficiency virus type 1 (HIV-1) are thought to be established by a single virus particle or genome. This means the viral population infecting a patient starts with virtually no genetic variation whatsoever. And without genetic variation, there’s no scope for evolution. That’s why the extremely rapid adaptation of the virus to the earliest immune responses is so puzzling.
How does the virus do it?
In the most recent issue of Genetics, I report on an investigation into the evolutionary dynamics behind HIV’s rapid adaptation.
I used a mathematical model of a virus population infecting a patient coded into a computer program to simulate viral evolution. The model includes only those components of the system that are thought to be critical to understanding the phenomenon.
In this case, the most important of the