Journal
JOURNAL OF VIRAL HEPATITIS
Volume 25, Issue 8, Pages 986-995Publisher
WILEY
DOI: 10.1111/jvh.12890
Keywords
acute infection; genotype 1; genotype 3; hepatitis E virus; host immune response-related genes; rhesus macaques
Funding
- National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, CDC
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Hepatitis E virus (HEV) genotype (gt) 3 infection is food-borne causing sporadic infections in older individuals and gt1 infection is waterborne, often causing epidemics affecting primarily young adults. Although HEV infection causes self-limited disease, gt3 induces chronic infection in immunocompromised individuals. Hepatic host gene expression against gt3 infection remains unknown. Host gene expression profiles for HEV gt1 (n=3) and gt3 (n=7) infections were analysed in the livers of experimentally infected rhesus macaques. HEV RNA was detected from 2 to 24days after inoculation (DAI) in stool and serum, elevated alanine aminotransferase (ALT) activity was detected from 7 to 31 DAI, and anti-HEV antibody became detectable between 12 and 42 DAI. All 10 animals cleared the infection between 34 and 68 DAI. We found that 24%, 48% and 41% of hepatic immune response genes against gt3 infection were upregulated during the early, peak and decline phases of HEV RNA replication. For gt1 infection, 25% of hepatic immune response-related genes were downregulated during early viremia, but 6%, 34% and 37% of genes were upregulated at the early, peak and during decline of HEV RNA replication, respectively. Our study demonstrated distinct differences in the expression profiles of host immune response-related genes of HEV gt3 and gt1 infections in experimentally infected rhesus macaques.
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