The recombination analysis of Y2 quasi-species showed variable types of recombinant between genotype C2, D1 and CD1 in 2006. Some studies show that hotspots of recombination most on the boundary of ORFs [12, 20] . Our results showed that two or more strains of HBV can recombine with each other at any region along the genome. Crossover regions can be hundreds or just several base pairs, The length of crossover region is depends on the location of it on HBV genome. If it is located in a conserved HBV region, for another word, where many different genotypes share the same sequence, the length of crossover region may be long. If it is located in a non-conserved region, it may be very short. At the same time, we found that the crossover region distributed totally at random on HBV genome. Consistent with our results, in vitro evidence showed the initial recombination events in a laboratory system of MHV were almost entirely randomly distributed along the sequence [21] . It was only after passage through cell culture, with the opportunity for selection to remove less fit variants, that crossover sites became ''localized'' to just a small area of the region examined. Crucially, they also suggested initial products of recombination may go undetected because of the action of strong purifying selection which will remove new, deleterious combinations of mutations. The conclusion is therefore an interpretation for the genotype change of Y2. The Y2 presented multiple strain infections of C2/D1/CD1 and many new recombinants with no obvious dominant genotype strain in 2006. After 18 months, however, all the type C2 and CD recombinant strains disappeared while the D strain became dominant. A similar case of mixed HBV genotype infection in which one genotype was lost and another prevailed was previously described in patients with HBeAg seroconversion [4, 22] .