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Genome-Wide Transcriptome Analysis of CD36 Overexpression in HepG2.2.15 Cells to Explore Its Regulatory Role in Metabolism and the Hepatitis B Virus Life Cycle.

ABSTRACT: Hepatitis B virus (HBV) is a hepatocyte-specific DNA virus whose gene expression and replication are closely associated with hepatic metabolic processes. Thus, a potential anti-viral strategy is to target the host metabolic factors necessary for HBV gene expression and replication. Recent studies revealed that fatty acid translocase CD36 is involved in the replication, assembly, storage, and secretion of certain viruses, such as hepatitis C virus (HCV) and human immunodeficiency virus (HIV). However, the relationship between CD36 and the HBV life cycle remains unclear. Here, we showed, for the first time, that increased CD36 expression enhances HBV replication in HepG2.2.15 cells. To understand the underlying molecular basis, we performed genome-wide sequencing of the mRNA from HepG2.2.15-CD36 overexpression (CD36OE) cells and HepG2.2.15-vector cells using RNA Sequencing (RNA-seq) technology to analyze the differential transcriptomic profile. Our results identified 141 differentially expressed genes (DEGs) related to CD36 overexpression, including 79 upregulated genes and 62 downregulated genes. Gene ontology and KEGG pathway analysis revealed that some of the DEGs were involved in various metabolic processes and the HBV life cycle. The reliability of the RNA-Seq data was confirmed by qPCR analysis. Our findings provide clues to build a link between CD36, host metabolism and the HBV life cycle and identified areas that require further investigation.

SUBMITTER: Huang J

PROVIDER: S-EPMC5066966 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Genome-wide Transcriptome Analysis of CD36 Overexpression in HepG2.2.15 Cells to Explore Its Regulation Role of Metabolism and HBV Life Cycle

Project description:To understand the molecular basis underlying the response to increasing CD36 overexpression in HepG2.2.15 cell, we performed genome-wide sequencing of the mRNAs from HepG2.2.15-CD36OE cell and HepG2.2.15-vector cell using the RNA-seq technology to detect its differential transcriptomic profile.

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Project description:Hepatitis E virus (HEV) is transmitted primarily via contaminated water and food by the fecal oral route and causes epidemics in developing countries. In industrialized countries, zoonotic transmission of HEV is prevalent. In addition, HEV is the major cause of acute hepatitis in healthy adults and can cause chronic hepatitis in immunocompromised patients, with pregnant HEV-infected women having increased mortality rates of approximately 25%. HEV was once an understudied and neglected virus. However, in recent years, the safety of blood products with respect to HEV has increasingly been considered to be a public health problem. The establishment of HEV infection models has enabled significant progress to be made in understanding its life cycle. HEV infects cells via a receptor (complex) that has yet to be identified. The HEV replication cycle is initiated immediately after the (+) stranded RNA genome is released into the cell cytosol. Subsequently, infectious viral particles are released by the ESCRT complex as quasi-enveloped viruses (eHEVs) into the serum, whereas feces and urine contain only nonenveloped infectious viral progeny. The uncoating of the viral envelope takes place in the biliary tract, resulting in the generation of a nonenveloped virus that is more resistant to environmental stress and possesses a higher infectivity than that of eHEV. This review summarizes the current knowledge regarding the HEV life cycle, viral morphogenesis, established model systems and vaccine development.

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Project description:Chronic infection with hepatitis B virus (HBV) increases the risk of developing fibrosis, cirrhosis or hepatocellular carcinoma. Current therapies are limited to type-I interferons and/or nucleos(t)ide analogues; however, these are only partially effective. The development of novel anti-HBV agents for new treatment strategies has been hampered by the lack of a suitable system that allows the in vitro replication of HBV. Studies of virus infection/replication at the molecular level using wild-type HBV are labor-intensive and time-consuming. To overcome these problems, we previously constructed a recombinant reporter HBV bearing the NanoLuc gene and showed its usefulness in identifying factors that affect HBV proliferation. Because this system mimics the early stage of the HBV life cycle faithfully, we conducted a quantitative analysis of HBV infectivity to several human hepatocyte cell lines as well as the effect of dimethyl sulfoxide and HBV protein X on the early stage of HBV proliferation using this system. Furthermore, we developed a system to produce a reporter HBV expressing a pol gene. These reporter HBV may provide an opportunity to enhance our understanding of the HBV life cycle and aid strategies for the development of new anti-HBV agents.

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Project description:To study the underlying molecular mechanisms during the Varroa destructor life cycle, we carried out transcriptomic profiling of seven stages: young mites (collected from P8 to P9 brood cells), phoretic mites (collected on adult bees), arresting mites (collected in unsealed L5 brood cells), pre-laying mites (collected from sealed brood cells containing moving larva), laying mites (collected from sealed brood cells containing pre-pupae), post-laying mites (collected from capped brood cells containing purple-eye and white-body pupae P5), emerging mites (collected from P8 to P9 brood cells). In addition, we sampled non-reproducing mites (collected from P5 brood cells, but without offspring), males (collected from P8 to P9 brood cells), and phoretic mites artificially reared in cages with adult bees. This study was performed using Apis mellifera L. honey bee colonies naturally infested by Varroa destructor mites. Adult mites were collected from 4 unrelated colonies.

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IFN-CSP inhibiting hepatitis B virus in HepG2.2.15 cells involves JAK-STAT signal pathway.

Project description:Frequent and high-dose administration of interferon to patients with viral hepatitis results in various side effects. In our previous study, a novel liver-targeting interferon (IFN-CSP) combining Plasmodium region I peptide with IFN?2b was successfully designed and expressed in the Escherichia coli expression systems. This targeting would target the IFN?2b specifically to the liver, thus reducing the adverse events. In the present study, we further investigated the anti-HBV effects and molecular mechanisms of recombinant IFN-CSP in HepG2.2.15 cell line. Hepatitis B surface antigen (HBsAg) and HBe antigen (HBeAg) in the culture supernatants were analyzed by enzyme-linked immunosorbent assay (ELISA). HBV-DNA was measured by real-time quantitative PCR. HBV core protein was assayed by immunofluorescent and western blot analysis. The expressions of signal transducers and transactivator 1 (STAT1), STAT2, IFN regulatory factor 9 (IRF-9), and 2'-5'-oligoadenylate synthetase 1 (OAS1) were investigated by the reverse transcription PCR and western blot analysis. Results indicate IFN-CSP efficiently inhibited HBsAg and HBeAg secretion, HBV-DNA replication, and HBV core protein expression in HepG2.2.15 cells. The anti-HBV mechanisms involve activation of JAK-STAT signaling and increase of the anti-HBV protein OAS expression. IFN-CSP could be a good substitute for IFN?2b for anti-HBV treatment.

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Project description:Deoxynucleotide triphosphates (dNTPs) are essential for efficient hepatitis B virus (HBV) replication. Here, we investigated the influence of the restriction factor SAMHD1, a dNTP hydrolase (dNTPase) and RNase, on HBV replication. We demonstrated that silencing of SAMHD1 in hepatic cells increased HBV replication, while overexpression had the opposite effect. SAMHD1 significantly affected the levels of extracellular viral DNA as well as intracellular reverse transcription products, without affecting HBV RNAs or cccDNA. SAMHD1 mutations that interfere with the dNTPase activity (D137N) or in the catalytic center of the histidine-aspartate (HD) domain (D311A), and a phospho-mimetic mutation (T592E), abrogated the inhibitory activity. In contrast, a mutation diminishing the potential RNase but not dNTPase activity (Q548A) and a mutation disabling phosphorylation (T592A) did not affect antiviral activity. Moreover, HBV restriction by SAMHD1 was rescued by addition of deoxynucleosides. Although HBV infection did not directly affect protein level or phosphorylation of SAMHD1, the virus upregulated intracellular dATPs. Interestingly, SAMHD1 was dephosphorylated, thus in a potentially antiviral-active state, in primary human hepatocytes. Furthermore, SAMHD1 was upregulated by type I and II interferons in hepatic cells. These results suggest that SAMHD1 is a relevant restriction factor for HBV and restricts reverse transcription through its dNTPase activity.

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