2009
DOI: 10.1111/j.1365-2613.2009.00699.x
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Abstract: This work studied the replication sites of hepatitis A virus (HAV) in cynomolgus monkeys (Macaca fascicularis) after intravenous inoculation. The cynomolgus monkeys were inoculated with the Brazilian hepatitis A virus strain (HAF-203). Monkeys were euthanized on days 15, 30, 45 and 60 postinoculation (pi). Liver samples, submandibular salivary gland, mesenteric lymph node and tonsils were removed for virological and pathological evaluation. Immunofluorescence analyses on liver and salivary gland sections using… Show more

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Cited by 34 publications
(32 citation statements)
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“…Therefore, in addition to the transudation of HAV‐containing fluid from the general circulation into the saliva through gengivo‐crevicular fluid, there may be other sources of HAV in saliva, including active viral replication at the site of salivary secretion in some individuals, as has been suggested for hepatitis C virus infections [Takamatsu et al, 1992; Roy et al, 1998; Arrieta et al, 2001]. HAV negative‐strand RNA (intermediate replicative) could be detected in the salivary glands of non‐human primates experimentally infected with HAV, demonstrating active HAV replication at this site [Amado et al, 2010]. Therefore, active HAV replication in the salivary glands would perhaps explain the discrepant subgenotypes between matched serum and saliva specimens.…”
Section: Discussionmentioning
confidence: 80%
“…Therefore, in addition to the transudation of HAV‐containing fluid from the general circulation into the saliva through gengivo‐crevicular fluid, there may be other sources of HAV in saliva, including active viral replication at the site of salivary secretion in some individuals, as has been suggested for hepatitis C virus infections [Takamatsu et al, 1992; Roy et al, 1998; Arrieta et al, 2001]. HAV negative‐strand RNA (intermediate replicative) could be detected in the salivary glands of non‐human primates experimentally infected with HAV, demonstrating active HAV replication at this site [Amado et al, 2010]. Therefore, active HAV replication in the salivary glands would perhaps explain the discrepant subgenotypes between matched serum and saliva specimens.…”
Section: Discussionmentioning
confidence: 80%
“…1). Viral RNA was reported recently to be present in the liver of cynomolgous monkeys as late as 9 wk after experimental HAV infection (40,41), but its continued presence beyond 46 wk in the chimpanzee (Fig. 1) was unexpected and represents another major difference from acute resolving hepatitis C. In acute resolving HCV infection, viral RNA is typically cleared by 10-20 wk of infection (Fig.…”
Section: Discussionmentioning
confidence: 92%
“…The high detection rates (33–42%) and mean concentrations that were observed for HAV at Maden Dam (1.72 × 10 4 genome copies/L) and Rooikrantz Dam (1.49 × 10 4 genome copies/L) are unexpected, considering the very low human population densities of the catchments of the two dams. However, HAV has been shown to cause acute hepatitis, not only in humans but also in some primates [36,69,70], and the bushy and mountainous catchments of the two dams were observed to host a high population of monkeys. The sequence alignment of target regions of the primers and probe used in this study proved them to be adequate for the quantification of all HAV genotypes [56].…”
Section: Resultsmentioning
confidence: 99%