Kowalik and Jensen (1) have reported that intra-host variation in HCMV approaches levels similar to
those of HCV, with fast mutation rates mooted as one explanation (2).While we discussed that HCMV
mutation rates were postulated as an explanation for high diversity, the focus of our work is on
observed inconsistencies in nucleotide diversity between and within patients (3). Kowalik and Jensen did
calculate HCMV mutation rates to be similar to MCMV but maintained that this could underestimate the
true levels (2). In contrast, our study showed that in the absence of mixed infections, HCMV is no more
diverse than other DNA viruses, and considerably less so than chronic RNA viruses. This simple
conclusion is different to that of Kowalik and Jensen and had not been stated prior to our publication.N
