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Báo cáo y học: "Gene expression profiling of monkeypox virus-infected cells reveals novel interfaces for host-virus interactions"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Gene expression profiling of monkeypox virus-infected cells reveals novel interfaces for host-virus interactions | Alkhalil et al. Virology Journal 2010 7 173 http www.virologyj.eom content 7 1 173 VIROLOGY JOURNAL RESEARCH Open Access Gene expression profiling of monkeypox virus-infected cells reveals novel interfaces for host-virus interactions 1 2 1 12 1 Abdulnaser Alkhalil Rasha Hammamieh Justin Hardick Mohamed Ait Ichou Marti Jett Sofi Ibrahim Abstract Monkeypox virus MPV is a zoonotic Orthopoxvirus and a potential biothreat agent that causes human disease with varying morbidity and mortality. Members of the Orthopoxvirus genus have been shown to suppress antiviral cell defenses exploit host cell machinery and delay infection-induced cell death. However a comprehensive study of all host genes and virus-targeted host networks during infection is lacking. To better understand viral strategies adopted in manipulating routine host biology on global scale we investigated the effect of MPV infection on Macaca mulatta kidney epithelial cells MK2 using GeneChip rhesus macaque genome microarrays. Functional analysis of genes differentially expressed at 3 and 7 hours post infection showed distinctive regulation of canonical pathways and networks. While the majority of modulated histone-encoding genes exhibited sharp copy number increases many of its transcription regulators were substantially suppressed suggesting involvement of unknown viral factors in host histone expression. In agreement with known viral dependence on actin in motility egress and infection of adjacent cells our results showed extensive regulation of genes usually involved in controlling actin expression dynamics. Similarly a substantial ratio of genes contributing to cell cycle checkpoints exhibited concerted regulation that favors cell cycle progression in G1 S G2 phases but arrest cells in G2 phase and inhibits entry into mitosis. Moreover the data showed that large number of infection-regulated genes is involved in molecular mechanisms characteristic of cancer canonical pathways. Interestingly ten ion channels