Epidemiologically, HBV genotype CD1 and C2 are the most common strains in ethnic minorities of northwest China with CD2 and D1 as minor strains. Precise mapping of recombination suggests C2 and D1 are parental sequences of CD1 and CD2 recombinants. Virological differences among HBV genotypes were demonstrated in vitroand in CHiM mice, with genotype C having a higher replication capacity than D [23] . Why does the replication-deficient genotype D virus predominate over replication-competent genotype C? As mixed HBV infections together with recombination are rare, we have little knowledge about i this situation. On the one hand, we know little about host impact on different genotypes and recombinants. On the other hand, we know little about interference and competition in the quasispecies of mixed infection. In vitro results showed the replication capacity of individual clone, exclude the influence of host and other strains of quasi-species. An example from a ChiM mice study showed that monoinfection of HBV/G in ChiM mice display a very slow replication while coinfection with HBV/A remarkably enhanced the replication of HBV/G. The replication of HBV/G is heavily dependent on coinfection with other genotypes. When HBV/G superinfected on other genotypes, a rapidly takes over of HBV/G from original genotype were observed, though they are indispensable [24] . This study confirms that in a mixed infection system of different genotypes, the replication capacity of a genotype may be different from that of monoinfection. At the same time, replication capacity is not the only factor to influence which strain will become dominant. Variable recombinants found in our study may be mechanistically capable of genetic exchange, but strong selection guaranteed the elimination of hybrid genomes. The mechanism of selection in mixed infection also needs more investigation.