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Hepatitis B virus surface gene variation: Just skin deep or profoundly pathogenic?

is not possible to draw firm conclusions. Second is the cross-sectional nature of the study, again recognized by the authors as a limiting factor. Hepatitis B virus likely exists as a quasispecies, with only major variants being detected by the technique of PCR sequencing. The relative proportion of these variants is likely to fluctuate over time and is likely to be dependent on the selective pressures operative at any given moment. Prospective data that are correlated with clinical, therapeutic, hostgenetic and other data that are likely to influence the host environment would be much more convincing. Third, is the difficulty involved in relating molecular genetic data to conventional serological profiles. The latter, as parameters of the traditional paradigm of understanding HBV infection, are useful up to a point, but are likely to become increasingly unhelpful in understanding the pathogenesis of infection at a molecular level. Related to this are issues of analytical sensitivity and specificity of diagnostic assays. It would be important to relate the antigenic specificity of the assays used to the epitopes that were sequenced when concluding that mutations thereof are significant. Fourth, one must be cautious before extrapolating outcome based on biochemical measurements taken at a single moment. On a more general level, it remains to be determined what one means when one uses terms such as ‘mutant’ and ‘variant’. These terms have meaning only in relationship to what may be considered ‘normal’ for a given population. One would have to determine what the normal virus is before deciding if a particular mutation is really a mutation. The attempt to associate point mutations with outcome is further complicated by the presence of mutations elsewhere in the genome that may affect replicative capacity or the capacity to evade or downregulate the host immune response. Some wellknown point mutations are related to the genotype. 5