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Experimental evidence of hepatitis A virus infection in pigs

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Hepatitis A virus (HAV) is the leading cause of acute viral hepatitis worldwide, with HAV infection being restricted to humans and nonhuman primates. In this study, HAV infection status was serologically determined in domestic pigs and experimental infections of HAV were attempted to verify HAV infectivity in pigs. Antibodies specific to HAV or HAV‐like agents were detected in 3.5% of serum samples collected from pigs in swine farms. When the pigs were infected intravenously with 2 × 105 50% tissue culture infectious dose (TCID50) of HAV, shedding of the virus in feces, viremia, and seroconversion were detected. In pigs orally infected with the same quantity of HAV, viral shedding was detected only in feces. HAV genomic RNA was detected in the liver and bile of intravenously infected pigs, but only in the bile of orally infected pigs. In further experiments, pigs were intravenously infected with 6 × 105 TCID50 of HAV. Shedding of HAV in feces, along with viremia and seroconversion, were confirmed in infected pigs but not in sentinel pigs. HAV genomic RNA was detected in the liver, bile, spleen, lymph node, and kidney of the infected pigs. HAV antigenomic RNA was detected in the spleen of one HAV‐infected pig, suggesting HAV replication in splenic cells. Infiltration of inflammatory cells was observed in the livers of infected pigs but not in controls. This is the first experimental evidence to demonstrate that human HAV strains can infect pigs. J. Med. Virol. 88:631–638, 2016. © 2015 Wiley Periodicals, Inc.
Title: Experimental evidence of hepatitis A virus infection in pigs
Description:
Hepatitis A virus (HAV) is the leading cause of acute viral hepatitis worldwide, with HAV infection being restricted to humans and nonhuman primates.
In this study, HAV infection status was serologically determined in domestic pigs and experimental infections of HAV were attempted to verify HAV infectivity in pigs.
Antibodies specific to HAV or HAV‐like agents were detected in 3.
5% of serum samples collected from pigs in swine farms.
When the pigs were infected intravenously with 2 × 105 50% tissue culture infectious dose (TCID50) of HAV, shedding of the virus in feces, viremia, and seroconversion were detected.
In pigs orally infected with the same quantity of HAV, viral shedding was detected only in feces.
HAV genomic RNA was detected in the liver and bile of intravenously infected pigs, but only in the bile of orally infected pigs.
In further experiments, pigs were intravenously infected with 6 × 105 TCID50 of HAV.
Shedding of HAV in feces, along with viremia and seroconversion, were confirmed in infected pigs but not in sentinel pigs.
HAV genomic RNA was detected in the liver, bile, spleen, lymph node, and kidney of the infected pigs.
HAV antigenomic RNA was detected in the spleen of one HAV‐infected pig, suggesting HAV replication in splenic cells.
Infiltration of inflammatory cells was observed in the livers of infected pigs but not in controls.
This is the first experimental evidence to demonstrate that human HAV strains can infect pigs.
J.
Med.
Virol.
88:631–638, 2016.
© 2015 Wiley Periodicals, Inc.

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