Orf virus ORF047 gene eukaryotic expression and cell localization / 中国人兽共患病学报

The object of study was to clone the gene of ORFV ORF047 and study the eukaryotic expression and cell localization,making the theoretical basis for the subsequest screening of protein that interact with ORF047.ORF047 gene was amplificated by the specifical primer from the DNA of ORFV using PCR,the length was 735 bp,compared with L1 published in NC-005336.1,the homologies of the nucleotide acid sequence and amino acid sequence were 98.8％ and 98.8％.In order to defined the expression and location of the ORF047 gene in cell,the recombinant plasmid pEGFP-ORF047 was constructed and transfected into 293T cell,after 36 h,the green fluorescence could be observed under fluorescence microscope,and 54 kD protein was detected by western bloting.The plasmid of pHcRed1-Nuc,pHcRed1-Mito and pHcRed1-ER with the recombinant plasmid of pEGFP-ORF047 was cotransfected to veroE6 cell respectively,that fusion protein of ORF047 was mainly located in the cytoplasm,a small amount in the mitochondriabyconfocal microscopy analysis.

Progress on host range factors and their mechanisms of poxvirus / 病毒学报

Poxvirus is one of the most serious zoonosis pathogens, which has largest genome and broadest host spectrum. With the development of molecular biology, functional genomics, and immunology-related technology, the interactions between pathogen and the host, particularly a large array of host range factors and their functions have been increasingly discovered. These findings provide references for the molecular basis of poxvirus tissue tropism and host specificity. This review focus on the introduction of host range factors in major members of Chordopoxvirinae to highlight the understanding of the mechanisms of molecular genetic evolution, the host tropism, and cross-species infection of poxviruses.

Modulation of the host toll-like receptor signaling pathways by virus infection / 病毒学报

Toll-like receptors (TLRs) are germline-encoded pattern recognition receptors (PRRs) that play a central role in host cell recognition and responses to virus infection, leading to the production of interferons (IFNs) and proinflammatory cytokines. In parallel, in order to establish an infection, viruses have to develop exclusively strategies to interfere with TLRs signaling, particularly some important adaptors activation such as MyD88, NF-kappaB, TRIF and IRFs, and suppress or escape host's antiviral immune response. In this paper, we review the latest findings on the various strategies used by viruses to modulate TLRs-mediated innate immune response, with special emphasis on immune evasion mechanism of VACV, HCV and HIV. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses hamper TLRs signaling and how to overcome viral infection.

The expression and imprinting status of insulin-like growth factor 2 gene in colorectal cancer / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To study the imprinting status and expression level of insulin-like growth factor 2 (IGF2) gene in colorectal cancer and to provide a clue for the mechanism of carcinogenesis of colorectal cancer.</p><p><b>METHODS</b>The expression levels of IGF2 in the paired colorectal cancer and adjacent normal tissue were examined and compared by use of semi-quantitative reverse transcription-polymerase chain reaction. The imprinting status of IGF2 was detected by restriction fragment length polymorphism. The relationships between the expression level of IGF2, its imprinting status, and the carcinogenesis of colorectal cancer were analyzed.</p><p><b>RESULTS</b>IGF2 was overexpressed in 82.4% (28/34) of colorectal cancer tissues which was significantly higher than those of the matched normal tissues (P<0.01, t=3.01). 87.5% (14/16) of colorectal cancer showed loss of imprinting(LOI), while 71.4%(10/14) of normal tissues also displayed LOI of IGF2.</p><p><b>CONCLUSION</b>Overexpression of IGF2 was found to play an important role in carcinogenesis of colorectal cancer. LOI of IGF2 may be a prophase manifestation of colorectal cancer.</p>