Alb-PSX transgenic line 107-5D mice (also called Tg[Alb-1,HBV]Bri66; inbred B10D2, H-2d) express nontoxic quantities of the three hepatitis B virus envelope/surface antigen proteins (large, middle, and small; all containing hepatitis B surface antigen (HBsAg) determinants) in their hepatocytes, are immunologically tolerant to HBsAg at the T cell level, and display no evidence of spontaneous liver disease nor hepatocellular carcinoma during their lifetime. 
 During the normal HBV replication cycle, the middle and small envelope proteins assemble to form the HBV major envelope polypeptide (a 22 nm spherical subviral particle containing HBsAg) that is rapidly-secreted secreted by the hepatocyte into the circulation. However, the ability of the hepatocytes to secrete these HBsAg subviral particles is inversely proportional to the abundance of the large envelope protein which, when coexpressed with the middle and small envelope proteins, forms long non-secretable filamentous particles that accumulate in the endoplasmic reticulum (where they are readily detectable immunohistochemically), thus precluding secretion of the 22 nm spherical forms.
 The Alb-PSX transgene is designed to have the mouse albumin promoter sequences directing expression of the HBV large envelope protein, but expression of the middle and small envelope proteins are regulated by a constitutively active internal promoter located within the envelope coding region on the transgene. Therefore, the albumin-promoter driven hepatocellular expression of the large envelope polypeptide results in the formation and retention of the non-secretable filamentous HBsAg particle in the hepatocyte endoplasmic reticulum (where it is detectable principally as cytoplasmic HBsAg in periportal hepatocytes close to the point of entry of the circulation into the hepatic lobule) and gives the hepatocytes a "ground glass" appearance. This renders the hepatocytes highly susceptible to destruction (MHC class I-restricted necro-inflammatory liver disease) after immune system ablation with subsequent adoptive transfer of HBsAg-specific cytotoxic T lymphocytes (CTLs). 
 Alb-PSX transgenic line 107-5D mice exhibit no detectable liver expression (RNA or protein) from the transgenic HBV X gene.
 Hemizygous mice are viable, fertile and healthy. To date (July 2015), it has not been attempted to make this strain homozygous.

Importantly, the donating investigator confirms that the Alb-PSX transgenic line 107-5D mice do not produce the infectious HBV particle (hepatitis B virion aka Dane particle). This is because the Alb-PSX transgene does not have the sequences encoding the viral DNA polymerase (P gene) or the HBV core protein (pre-C [HBeAg] and C gene [HBcAg]).

Alb-PSX transgenic line 107-5D mice (also called Tg[Alb-1,HBV]Bri66; inbred B10D2, H-2d) have the mouse albumin promoter sequences directing expression of the envelope/surface antigen coding region (HBsAg) of the hepatitis B virus (HBV). This results in retention of the non-secretable filamentous HBsAg particle in the hepatocyte endoplasmic reticulum; with little-to-no HBsAg secretion into serum. These mice are a model for studying the immunopathogenesis of acute T cell mediated hepatitis, chronic T cell mediated hepatitis, and the downstream consequences of chronic hepatitis, especially hepatocellular carcinoma.

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