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Gene expression profile in human skeletal muscle cells infected with human adenovirus type 36
Author(s) -
Wang Zhong Q.,
Yu Yongmei,
Zhang Xian H.,
Qin Jianhua,
Floyd Elizabeth
Publication year - 2012
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.23332
Subject(s) - virology , biology , gene , skeletal muscle , adenoviridae , genetic enhancement , gene expression , virus , microbiology and biotechnology , genetics , anatomy
Human adenovirus type‐36 (HAdV‐36) is a specific pathogen that may lead to increased adiposity and obesity. In order to evaluate the effects of HAdV‐36 on gene transcription, a microarray analysis of muscle cells infected with HAdV‐36 was performed. Gene expression profile was determined by microarray analysis in cultured human skeletal muscle cells with or without HAdV‐36 infection. Quantitative real‐time PCR (qPCR) assay was performed in selected 35 genes to verify the results of the microarray analysis. A total of 13,060 unique genes were detected in the HAdV‐36 infected muscle cells infected with HAdV‐36. Among them, 1,004 genes were significantly altered by using a cut‐off point at fold change ≥1.5 and P value <0.05. Most of the principal 100 altered genes were involved in development, immune response, signal transduction, transcriptional regulation as well as carbohydrate, lipid and protein metabolism. Thirty‐two genes (91.4%) from the 35 selected genes were confirmed by qPCR assay. In addition, HAdV‐36 altered 252 genes that are associated with cancer. The study showed HAdV‐36 infection upregulated host cell antiviral defense. HAdV‐36 also induces changes in gene expression related to cellular signaling pathways of signal transduction, transcriptional regulation as well as carbohydrate, lipid and protein metabolism. However, it remains to be investigated if HAdV‐36 infection could lead to oncogenesis. J. Med. Virol. 84: 1254–1266, 2012. © 2012 Wiley Periodicals, Inc.