Abstract
Highly pathogenic fowl adenovirus serotype 4 (FAdV-4) is the causative agent of hydropericardium syndrome (HPS), which is characterized by pericardial effusion and hepatitis, and is one of the foremost causes of economic losses to the poultry industry over the last 30 years. However, the metabolic changes in cells in response to FAdV-4 infection remain unclear. In order to understand the metabolic interactions between the host cell and virus, we utilized ultra-high-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry to analyze the metabolic profiles with hepatocellular carcinoma cell line (LMH) infected with FAdV-4. The results showed that FAdV-4 could restore metabolic networks in LMH cells and tricarboxylic acid cycle, glycolysis, and metabolism of purines, pyrimidines, alanine, aspartate, glutamate, and amino sugar and nucleotide sugar moieties. Moreover, FAdV-4 production was significantly reduced in LMH cells cultured in glucose or glutamine-deficient medium. These observations highlighted the importance of host cell metabolism in virus replication. Therefore, similarities and disparities in FAdV-4-regulation of the metabolism of host cells could help improve targeted drug and reduce infection.
Highlights
Fowl adenovirus serotype 4 (FAdV-4) is a highly pathogenic hepatotropic virus and the etiological agent of hydropericardium syndrome (HPS), which is an infectious disease of broiler chickens characterized by pericardial effusion and acute hemorrhagic hepatitis, resulting in high mortality rates (Schachner et al, 2014; Steer et al, 2015; Zhao et al, 2015; Niu et al, 2018a,b; Wang and Zhao, 2019)
To elucidate the molecular mechanisms underlying the pathogenesis of fowl adenovirus serotype 4 (FAdV-4) infection, high throughput techniques can be used to reveal global changes in the expression profiles of gene and proteins associated with metabolism and disease progression
Indirect immunofluorescence showed that about 50% of the cells were infected with FAdV-4 at 24 hpi (Figure 1B), and hematoxylin and eosin staining confirmed the formation of viral inclusion bodies (Figure 1C)
Summary
Fowl adenovirus serotype 4 (FAdV-4) is a highly pathogenic hepatotropic virus and the etiological agent of hydropericardium syndrome (HPS), which is an infectious disease of broiler chickens characterized by pericardial effusion and acute hemorrhagic hepatitis, resulting in high mortality rates (Schachner et al, 2014; Steer et al, 2015; Zhao et al, 2015; Niu et al, 2018a,b; Wang and Zhao, 2019). The diagnostic criteria for HPS are relatively well established, the intrinsic mechanisms underlying FAdV-4 infection of host cells remain unclear. To elucidate the molecular mechanisms underlying the pathogenesis of FAdV-4 infection, high throughput techniques can be used to reveal global changes in the expression profiles of gene and proteins associated with metabolism and disease progression. Mounting evidence indicates that similarities and disparities in virus-induced regulation of host cell metabolism could help to improve the efficacy of targeted drug therapies and reduce the incidence of infection (Cui et al, 2013; Sun et al, 2013; Ni et al, 2014). Relatively few studies have investigated changes to host cell metabolomics in response to FAdV-4 infection. Metabolomics might be useful to elucidate the pathogenic mechanisms underlying FAdV-4 infection of hepatic cells
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