ABSTRACT
El virus de la hepatitis B (HBV) presenta amplia distribución en todo el mundo, con más de 500 millones de individuos infectados. Este microorganismo pertenece a la familia Hepadnaviridae. En el presente trabajo se analizó la presencia del antígeno de superficie del virus (HBsAg) y perfil enzimático (GOT, GPT y FAL) en 292 muestras de suero o plasma de estudiantes universitarios de ambos sexos. De las muestras analizadas una sola resultó "Reactiva" para el HBsAg, lo que representa el 0.34 %, confirmado por técnica de reacción en cadena de la polimerasa.
Summary The Hepatitis B virus (HBV) is widely distributed throughout the world, with more than 500 million infected individuals. Is a virus belonging to the Hepnaviridae family. In the present work was analyzed the presence of HBsAg and enzymatic profile (GOT, GPT, FAL) in 292 serum samples or plasm of university students of both sexes. From analyzed samples so far, only one of them was "reactive" for HBsAg, which represents 0,34%. In addition, the determination of total anti-core antibodies was realised to the latter sample resulting "reactive
Subject(s)
Hepadnaviridae , Hepatitis B virus , Antigens/analysisABSTRACT
BACKGROUND: CD8+ T cells contribute to the clearance of Hepatitis B virus (HBV) infection and an insufficient CD8+ T cell response may be one of the major factors leading to chronic HBV infection. Since the HBx antigen of HBV can up-regulate cellular expression of several immunomodulatory molecules, we hypothesized that HBx expression in hepatocytes might affect CD8+ T cell activity. METHODS: We analyzed the activation and apoptosis of CD8+ T cells co-cultured with primary hepatocytes rendered capable of expressing HBx by recombinant baculovirus infection. RESULTS: Expression of HBx in hepatocytes induced low production of interferon-gamma and apoptosis of CD8+ T cells, with no effect on CD8 T cell proliferation. However, transcriptional levels of H-2K, ICAM-1 and PD-1 ligand did not correlate with HBx expression in hepatocytes. CONCLUSION: Our results suggest that HBx may inhibit CD8+ T cell response by regulation of interferon-gamma production and apoptosis.
Subject(s)
Apoptosis , Baculoviridae , Cell Proliferation , Hepadnaviridae , Hepatitis , Hepatitis B , Hepatitis B virus , Hepatocytes , Intercellular Adhesion Molecule-1 , Interferon-gamma , T-Lymphocytes , Trans-Activators , Viral ProteinsABSTRACT
Entry and intracellular transport of hepatitis B viruses have several unusual, largely unknown aspects. In this study, we explored the mode of virus entry using the duck hepatitis B virus [DHBV] and the primary hepatocyte infection model. Upon internalization, viral particles were enriched in an endosomal compartment, as revealed by biochemical and ultrastructural analysis. Virus-containing vesicles harbored early endosome markers. Kinetic analysis revealed time-dependent partial translocation of viral DNA from endosomes into the cytosol. This was strongly reduced by inhibition of vacuolar ATPase; [vATPase] activity with bafilomycin A1 and resulted in abortive infection and prevention of cccDNA formation. Inactivation of vATPase induced accumulation and stabilization of incoming viral particles in endosomes, presumably by blocking endosomal carrier vesicle-mediated cargo transport and sorting. Although neutralization of the endomembrane organelles alone led to stabilization of incoming viral particles, it did not inhibit virus infection. In line with this, a pH-dependent ectopic virus fusion at the plasma membrane could not be artificially induced. This provided further evidence for a pH-neutral translocation mechanism. Endosomal membrane potential was required for viral infection because cotreatment of cells with monensin partially overcame the inhibitory effect of bafilomycin A1. In conclusion, hepatitis B viral infection is mediated by a novel cellular entry mechanism with features different from that of all other known viruses