Replies to post #50671 on Biotech Values

[rfj1862]

Not at all. In almost every infected individual there is already a population of virus that is dependent on CXCR4 for entry. No mutations necessary. In fact, if I remember correctly, HIV infections shift from a largely CCR5-dependent (macrophage-tropic) population early in infection to a CXCR4-dependent (T-cell tropic) population later in infection. Or the other way around, I can't remember.

Mutations occur on a genomic level. If every base has an equal probability of mutation (an oversimplification, of course) the potential for mutations is simply a function of target size.