into woodchucks with the delayed onset of HCC. Between humans and non-human mammals Since the similarity between human and apes, and common ancestors human and apes shared long time ago, there are possibilities to happen transmission of HBVs among them. The prevalence of HBV infection in the natural primate habitat is unknown. Most data resulted from the studies performed on samples obtained from captive animals, wild-born or captive-born. Human HBV infects only humans and closely related primates, such as chimpanzee, chacma baboon, and to some extent, tree shrew, but does not infect woolly monkeys. HBV isolates have been shown to infect gibbon apes and chimpanzees, but not convincing evidence of an infection of macaques or other members of the Cercopithecidea family. Macaca sylvanus is able to replicate HBV in vivo replication in primary macaque hepatocytes. However, susceptibility of these animals has not been shown. Gibbons: studies show that the vertical transmission is essential in the transmission of HBV in the non-human primates. But, there is also a possibility of horizontal transmission confirmed by HBV DNA detection in gibbon saliva. If the gibbons were housed in the same habitat, they would likely transmit HBV to the other gibbons through sexual contact or horizontal transmission of family members. Chimpanzees: viral hepatitis had been known to occur in captive chimpanzees even prior to the discovery of HBV. Many studies used the chimpanzee models which have been limited now, showed that shortly after the first cloning of the HBV genome, the cloned DNA was infectious in chimpanzees, mostly developed hepatic pathology similar to the acute HBV infection in human, but they did not develop a chronic liver disease. Tupaias: they are susceptible to the human HBV. However, the experimental infection is not highly efficient and causes only a mild, transient infection with low viral titers. Primary hepatocytes isolated from the liver of Tupaias are well susceptible to HBV infection. Mice: Several researchers developed transgenic mice in order to study the expression of coding regions for the surface antigens, products of preS, S, and X gene of HBVs. The transgenic mice were not susceptible to HBV, but mice with severe combined immunodeficiency (SCID) can develop chronic liver disease. In addition, they permitted HBV to replicate in human hepatocytes that were able to proliferate in these mice. In general, these results imply that nonhuman primate HBV variants may be transmittable to humans. At least they infect