Partial characterization and tissue distribution of the feline mu opiate receptor.

Heroin abuse is a common route of acquiring HIV-1 infection. However, the effects of opiates on lentivirus disease progression are not well understood. Feline immunodeficiency virus is recognized as a good animal model for HIV-1, but characterization of the opiate receptor system in cats is lacking. Here we report the partial sequencing of the feline mu opiate receptor (MOR) and demonstrate a homology of 92 and 93% to the published human MOR sequences. Additionally, MOR transcripts were detected in the feline brain and tonsil but not in the spleen. Also, specific receptor ligand interactions were observed using microphysiometry.

The hepatitis B virus X gene potentiates c-myc-induced liver oncogenesis in transgenic mice.

The hepatitis B virus X protein (HBx) is thought to be implicated in the development of hepatocellular carcinoma, but its exact function remains controversial. Transgenic mice from PEX7 and AX16 lineages that express HBx in the liver under control of different viral regulatory elements develop no liver pathology (Billet et al., 1995). We have crossed these two mouse lineages with WHV/c-myc oncomice in which liver-specific expression of c-myc driven by woodchuck hepatitis virus (WHV) regulatory sequences causes liver cancer in all animals. The average tumor latency was shortened by 2 to 3 months in bitransgenic animals from all populations compared with simple c-myc transgenic littermates. At preneoplastic stages, adult bitransgenic mice showed four to fivefold enhanced expression of the c-myc transgene, increased hepatocyte proliferation and more extensive liver lesions compared with simple WHV/c-myc transgenics. Thus in this model, HBx alone has no direct pathological effect but it is shown to accelerate tumor development induced by c-myc. The data presented here firmly establish the oncogenic potential of HBx, apparently acting as a tumor promoter. This model offers unique opportunities to investigate the mechanisms by which HBx trans-activates the expression of target genes and deregulates the hepatocyte growth control in vivo.

In vivo activity of the hepatitis B virus core promoter: tissue specificity and temporal regulation.

The contribution of the hepatitis B virus enhancers I and II in the regulation of the activity of the core and the X promoters was assessed in transgenic mice. Surprisingly, despite the presence of heterologous promoters linked 5' of the X gene, the transgene expression is mostly due to core promoter (Cp) activity present in the X coding sequence. Moreover, the restriction of Cp activity to hepatic tissue required the combined action of both enhancers I and II, whereas the proximity of these two enhancers was insufficient to confer tissue specificity on Xp activity. Furthermore, the liver-specific activity of the Cp was developmentally regulated in an enhancer I-independent manner.

Hepatitis B virus X gene product acts as a transactivator in vivo.

It has previously been shown that the hepatitis B virus X gene product, pX, transactivates homologous and heterologous transcriptional regulatory sequences of viruses and various cellular genes in vitro. However, there is no evidence about the reproducibility and the relevance of this phenomenon in vivo. In this study we crossbred transgenic mice expressing the X gene under the control of the human antithrombin III (ATIII) gene regulatory sequences with transgenics carrying either the chloramphenicol acetyl-transferase or the LacZ bacterial reporter genes driven by the HIV1-LTR, which is known to be activated in trans by pX. Expression of pX in the liver stimulates the HIV1-LTR driven expression of both chloramphenicol acetyl-transferase and beta-galactosidase reporter genes in double transgenic mice. No detectable increase in chloramphenicol acetyl-transferase expression was observed in tissues, such as the spleen, brain and heart, that do not express pX. Our results confirm the transactivating properties of pX in vivo for the first time and support the hypothesis that pX might indeed modify gene expression in HBV-infected hepatocytes and influence viral pathogenesis.

The hepatitis B virus X gene product transactivates the HIV-LTR in vivo.

It has previously been shown that the hepatitis B virus (HBV) X gene product, HBx, transactivates homologous and heterologous transcriptional regulatory sequences of viruses, including the human immunodeficiency virus type 1 (HIV1) long terminal repeat (LTR), and various cellular genes in vitro. To evaluate the transactivating function of HBx in vivo, we generated transgenic mice carrying the X open reading frame under the control of the human antithrombin III (ATIII) gene regulatory sequences. These mice express the 16 Kd HBx protein in the liver, as demonstrated by immunoprecipitation studies. Crossbreeding of HBx mice with transgenics carrying either the chloramphenicol acetyl transferase (CAT) bacterial or the lacZ reporter gene driven by the HIV1-LTR allowed us to demonstrate, for the first time, the in vivo transactivating function of HBx protein.

[Radiological and magnetic resonance aspects in cerebral venous angioma]. / Aspects radiologiques et en résonance magnétique des angiomes veineux cérébraux.

This report based on a series of 8 cases deals with the appearance of cerebral venous angiomas with computed tomography (CT), arteriography and magnetic resonance imaging (MRI). The CT data are not conclusive, and venous involvement is demonstrated by arteriography, as well as the site of involvement. Magnetic resonance imaging seems to be useful owing to the morphological information and data on flow phenomena it provides.