RESUMO
BACKGROUND: Hepatocellular carcinoma (HCC) may be caused by hepatitis B virus (HBV) infection. Post-infection recovery-associated changes of HBV indicators include decreased hepatitis B surface antigen (HBsAg) level and increased anti-HBsAg antibody titer. Testing to detect HBV DNA is conducted rarely but could detect latent HBV infection persisting after acute infection and prompt administration of treatments to clear HBV and prevent subsequent HBV-induced HCC development. Here, we present an HCC case with an extremely high anti-HBsAg antibody titer and latent HBV infection. CASE SUMMARY: A 57-year-old male patient with abdominal pain who was diagnosed with primary HCC presented with an extremely high level (over 2000 ng/mL) of serum alpha-fetoprotein. Abdominal B-ultrasonography and computed tomography scan results indicated focal liver lesion and mild splenomegaly. Assessments of serological markers revealed a high titer of antibodies against hepatitis B core antigen (anti-HBcAg antibodies), an extremely high titer (1000 mIU/mL) of hepatitis B surface antibodies (anti-HBsAg antibodies, anti-HBs) and absence of detectible HBsAg. Medical records indicated that the patient had reported no history of HBV vaccination, infection or hepatitis. Therefore, to rule out latent HBV infection in this patient, a serum sample was collected then tested to detect HBV DNA, yielding a positive result. Based on the aforementioned information, the final diagnosis was HCC associated with hepatitis B in a compensated stage of liver dysfunction and the patient was hospitalized for surgical treatment. CONCLUSION: A rare HCC case with high serum anti-HBsAg antibody titer and detectable HBV DNA resulted from untreated latent HBV infection.
RESUMO
Hepatitis E virus (HEV), a fecal-orally transmitted foodborne viral pathogen, causes acute hepatitis in humans and is responsible for hepatitis E outbreaks worldwide. Since the identification of HEV as a zoonotic agent, this virus has been isolated from a variety of hosts with an ever-expanding host range. HEV-open reading frame (ORF) 3, the smallest ORF in HEV genomes, initially had been perceived as an unremarkable HEV accessory protein. However, as novel HEV-ORF3 function has been discovered that is related to the existence of a putative third virion structural form, referred to as "quasi-enveloped" HEV particles, HEV is challenging the conventional virion structure-based classification scheme, which assigns all viruses to two groups, "enveloped" or "non-enveloped". In this review, we systematically describe recent progress that has identified multiple pathogenic roles of HEV-ORF3, including roles in HEV virion release, biogenesis of quasi-enveloped virus, regulation of the host innate immune response, and interference with host signaling pathways. In addition, implications of HEV-ORF3-associated quasi-enveloped virions are discussed to guide future development of improved vaccines against zoonotic HEV infection.