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Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures

BACKGROUND: The human hepatitis B virus (HBV), a member of the hepadna viridae, causes acute or chronic hepatitis B, and hepatocellular carcinoma (HCC). The duck hepatitis B virus (DHBV) infection, a dependable and reproducible model for hepadna viral studies, does not result in HCC unlike chronic H...

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Autores principales: Nair, Sajith, Arathy, Devaki S, Issac, Aneesh, Sreekumar, Easwaran
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3152538/
https://www.ncbi.nlm.nih.gov/pubmed/21781334
http://dx.doi.org/10.1186/1743-422X-8-363
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author Nair, Sajith
Arathy, Devaki S
Issac, Aneesh
Sreekumar, Easwaran
author_facet Nair, Sajith
Arathy, Devaki S
Issac, Aneesh
Sreekumar, Easwaran
author_sort Nair, Sajith
collection PubMed
description BACKGROUND: The human hepatitis B virus (HBV), a member of the hepadna viridae, causes acute or chronic hepatitis B, and hepatocellular carcinoma (HCC). The duck hepatitis B virus (DHBV) infection, a dependable and reproducible model for hepadna viral studies, does not result in HCC unlike chronic HBV infection. Information on differential gene expression in DHBV infection might help to compare corresponding changes during HBV infection, and to delineate the reasons for this difference. FINDINGS: A subtractive hybridization cDNA library screening of in vitro DHBV infected, cultured primary duck hepatocytes (PDH) identified cDNAs of 42 up-regulated and 36 down-regulated genes coding for proteins associated with signal transduction, cellular respiration, transcription, translation, ubiquitin/proteasome pathway, apoptosis, and membrane and cytoskeletal organization. Those coding for both novel as well as previously reported proteins in HBV/DHBV infection were present in the library. An inverse modulation of the cDNAs of ten proteins, reported to play role in human HCC, such as that of Y-box binding protein1, Platelet-activating factor acetylhydrolase isoform 1B, ribosomal protein L35a, Ferritin, α-enolase, Acid α-glucosidase and Caspase 3, copper-zinc superoxide dismutase (CuZnSOD), Filamin and Pyruvate dehydrogenase, was also observed in this in vitro study. CONCLUSIONS: The present study identified cDNAs of a number of genes that are differentially modulated in in vitro DHBV infection of primary duck hepatocytes. Further correlation of this differential gene expression in in vivo infection models would be valuable to understand the little known aspects of the hepadnavirus biology.
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spelling pubmed-31525382011-08-09 Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures Nair, Sajith Arathy, Devaki S Issac, Aneesh Sreekumar, Easwaran Virol J Short Report BACKGROUND: The human hepatitis B virus (HBV), a member of the hepadna viridae, causes acute or chronic hepatitis B, and hepatocellular carcinoma (HCC). The duck hepatitis B virus (DHBV) infection, a dependable and reproducible model for hepadna viral studies, does not result in HCC unlike chronic HBV infection. Information on differential gene expression in DHBV infection might help to compare corresponding changes during HBV infection, and to delineate the reasons for this difference. FINDINGS: A subtractive hybridization cDNA library screening of in vitro DHBV infected, cultured primary duck hepatocytes (PDH) identified cDNAs of 42 up-regulated and 36 down-regulated genes coding for proteins associated with signal transduction, cellular respiration, transcription, translation, ubiquitin/proteasome pathway, apoptosis, and membrane and cytoskeletal organization. Those coding for both novel as well as previously reported proteins in HBV/DHBV infection were present in the library. An inverse modulation of the cDNAs of ten proteins, reported to play role in human HCC, such as that of Y-box binding protein1, Platelet-activating factor acetylhydrolase isoform 1B, ribosomal protein L35a, Ferritin, α-enolase, Acid α-glucosidase and Caspase 3, copper-zinc superoxide dismutase (CuZnSOD), Filamin and Pyruvate dehydrogenase, was also observed in this in vitro study. CONCLUSIONS: The present study identified cDNAs of a number of genes that are differentially modulated in in vitro DHBV infection of primary duck hepatocytes. Further correlation of this differential gene expression in in vivo infection models would be valuable to understand the little known aspects of the hepadnavirus biology. BioMed Central 2011-07-23 /pmc/articles/PMC3152538/ /pubmed/21781334 http://dx.doi.org/10.1186/1743-422X-8-363 Text en Copyright ©2011 Nair et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Short Report
Nair, Sajith
Arathy, Devaki S
Issac, Aneesh
Sreekumar, Easwaran
Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures
title Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures
title_full Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures
title_fullStr Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures
title_full_unstemmed Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures
title_short Differential gene expression analysis of in vitro duck hepatitis B virus infected primary duck hepatocyte cultures
title_sort differential gene expression analysis of in vitro duck hepatitis b virus infected primary duck hepatocyte cultures
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3152538/
https://www.ncbi.nlm.nih.gov/pubmed/21781334
http://dx.doi.org/10.1186/1743-422X-8-363
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