Experimental hepatitis A virus (HAV) infection in Callithrix jacchus: Early detection of HAV antigen and viral fate

Pinto, Marcelo Alves; Marchevsky, Renato Sérgio; Baptista, Márcia L.; Lima, M.A. de; Pelajo-Machado, Marcelo; Vitral, Cláudia Lamarca; Kubelka, Claire Fernandes; Pissurno, J.W.; França, Monique; Schatzmayr, H. G.; Gaspar, Ana

doi:10.1078/0940-2993-00212

Cited by 32 publications

(35 citation statements)

References 23 publications

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“…Animal experiments have further shown that infectious virus is shed in saliva during the incubation period and in the early acute phase (2) and that HAV RNA may be detected in saliva from 6 h postinoculation until several weeks after hepatitis onset (6). We show here the frequent presence of HAV RNA in the saliva of acutely infected patients and we confirm by real-time PCR quantification a difference of about 2 logs between serum and saliva viral loads.…”

supporting

confidence: 70%

Detection of Hepatitis A Virus RNA in Saliva

et al. 2004

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supporting

confidence: 70%

Detection of Hepatitis A Virus RNA in Saliva

et al. 2004

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“…In experimentally infected marmosets (156,187), the viral load appears to be 1 to 3 log 10 units lower than that found in serum (156). However, no epidemiological data suggest that saliva is a significant source of HAV transmission.…”

Section: Pathogenesis and Natural History Of Hav Infectionmentioning

confidence: 92%

Diagnosis of Hepatitis A Virus Infection: a Molecular Approach

et al. 2006

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SUMMARY Current serologic tests provide the foundation for diagnosis of hepatitis A and hepatitis A virus (HAV) infection. Recent advances in methods to identify and characterize nucleic acid markers of viral infections have provided the foundation for the field of molecular epidemiology and increased our knowledge of the molecular biology and epidemiology of HAV. Although HAV is primarily shed in feces, there is a strong viremic phase during infection which has allowed easy access to virus isolates and the use of molecular markers to determine their genetic relatedness. Molecular epidemiologic studies have provided new information on the types and extent of HAV infection and transmission in the United States. In addition, these new diagnostic methods have provided tools for the rapid detection of food-borne HAV transmission and identification of the potential source of the food contamination.

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“…This direction of secretion in hepatocytes would result in the direct release of virus into the bile and gastrointestinal tract, as might be expected for enteric excretion (4). Indeed, there is good evidence in many primate studies showing HAV antigens present in the bile of infected animals with acute hepatitis A (26,29,34,34,42,48). However, in liver cells, direct apical transportation from the Golgi complex runs counter to the direction of export of most de novosynthesized substrates.…”

mentioning

confidence: 99%

Vectorial Entry and Release of Hepatitis A Virus in Polarized Human Hepatocytes

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Mackenzie

et al. 2008

J Virol

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Hepatitis A virus (HAV) is an enterically transmitted virus that replicates predominantly in hepatocytes within the liver before excretion via bile through feces. Hepatocytes are polarized epithelial cells, and it has been assumed that the virus load in bile results from direct export of HAV via the apical domain of polarized hepatocytes. We have developed a subclone of hepatocyte-derived HepG2 cells (clone N6) that maintains functional characteristics of polarized hepatocytes but displays morphology typical of columnar epithelial cells, rather than the complex morphology that is typical of hepatocytes. N6 cells form microcolonies of polarized cells when grown on glass and confluent monolayers of polarized cells on semipermeable membranes. When N6 microcolonies were exposed to HAV, infection was restricted to peripheral cells of polarized colonies, whereas all cells could be infected in colonies of nonpolarized HepG2 cells (clone C11) or following disruption of tight junctions in N6 colonies with EGTA. This suggests that viral entry occurs predominantly via the basolateral plasma membrane, consistent with uptake of virus from the bloodstream after enteric exposure, as expected. Viral export was also found to be markedly vectorial in N6 but not C11 cells. However, rather than being exported from the apical domain as expected, more than 95% of HAV was exported via the basolateral domain of N6 cells, suggesting that virus is first excreted from infected hepatocytes into the bloodstream rather than to the biliary tree. Enteric excretion of HAV may therefore rely on reuptake and transcytosis of progeny HAV across hepatocytes into the bile. These studies provide the first example of the interactions between viruses and polarized hepatocytes.

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Experimental hepatitis A virus (HAV) infection in Callithrix jacchus: Early detection of HAV antigen and viral fate

Cited by 32 publications

References 23 publications

Detection of Hepatitis A Virus RNA in Saliva

Detection of Hepatitis A Virus RNA in Saliva

Diagnosis of Hepatitis A Virus Infection: a Molecular Approach

Vectorial Entry and Release of Hepatitis A Virus in Polarized Human Hepatocytes

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