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评估格鲁吉亚分离株基因组中非洲猪瘟病毒基因的缺失。

Evaluation of the Deletion of the African Swine Fever Virus Gene from the Genome of the Georgia Isolate.

机构信息

Plum Island Animal Disease Center, ARS, USDA, Greenport, NY 11944, USA.

Oak Ridge Institute for Science and Education (ORISE), Oak Ridge, TN 37830, USA.

出版信息

Viruses. 2023 Oct 23;15(10):2134. doi: 10.3390/v15102134.

DOI:10.3390/v15102134
PMID:37896911
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10612027/
Abstract

African swine fever virus (ASFV) is a structurally complex, double-stranded DNA virus, which causes African swine fever (ASF), a contagious disease affecting swine. ASF is currently affecting pork production in a large geographical region, including Eurasia and the Caribbean. ASFV has a large genome, which harbors more than 160 genes, but most of these genes' functions have not been experimentally characterized. One of these genes is the gene which has been experimentally shown to function as a small DNA polymerase. Here, we demonstrate that the deletion of the gene from the genome of the virulent strain ASFV Georgia2010 (ASFV-G) does not significantly affect virus replication in vitro or in vivo. A recombinant virus, having deleted the gene, ASFV-G-∆O174L, was developed to study the effect of the protein in replication in swine macrophages cultures in vitro and disease production when inoculated in pigs. The results demonstrated that ASFV-G-∆O174L has similar replication kinetics to parental ASFV-G in swine macrophage cultures. In addition, animals intramuscularly inoculated with 10 HAD of ASFV-G-∆O174L presented a clinical form of the disease that is indistinguishable from that induced by the parental virulent strain ASFV-G. All animals developed a lethal disease, being euthanized around day 7 post-infection. Therefore, although O174L is a well-characterized DNA polymerase, its function is apparently not critical for the process of virus replication, both in vitro and in vivo, or for disease production in domestic pigs.

摘要

非洲猪瘟病毒(ASFV)是一种结构复杂的双链 DNA 病毒,可引起非洲猪瘟(ASF),这是一种影响猪的传染病。ASF 目前正在包括欧亚大陆和加勒比地区在内的大片地区影响猪肉生产。ASFV 具有庞大的基因组,其中包含 160 多个基因,但这些基因的大多数功能尚未通过实验进行表征。其中一个基因是 基因,该基因已通过实验证明具有小 DNA 聚合酶的功能。在这里,我们证明从强毒力菌株 ASFV Georgia2010(ASFV-G)的基因组中删除 基因不会显著影响病毒在体外或体内的复制。我们开发了一种缺失了 基因的重组病毒,ASFV-G-∆O174L,用于研究在体外猪巨噬细胞培养物中复制和接种猪时该 蛋白在疾病产生中的作用。结果表明,ASFV-G-∆O174L 在猪巨噬细胞培养物中的复制动力学与亲本 ASFV-G 相似。此外,用 10 HAD 的 ASFV-G-∆O174L 肌肉内接种的动物呈现出与亲本强毒力菌株 ASFV-G 诱导的疾病相似的临床形式。所有动物都患上了致命疾病,并在感染后第 7 天左右被安乐死。因此,尽管 O174L 是一种特征明确的 DNA 聚合酶,但它的功能显然对病毒在体外和体内的复制过程或在国内猪中的疾病产生不是至关重要的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/09bca1312456/viruses-15-02134-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/4a42577b05ea/viruses-15-02134-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/8051af0add04/viruses-15-02134-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/3b941cd2f9f3/viruses-15-02134-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/d0cb93e041c6/viruses-15-02134-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/b8bbd2325eea/viruses-15-02134-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/4ff6574eb63e/viruses-15-02134-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/dcb86e6b16c9/viruses-15-02134-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/09bca1312456/viruses-15-02134-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/4a42577b05ea/viruses-15-02134-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/8051af0add04/viruses-15-02134-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/3b941cd2f9f3/viruses-15-02134-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/d0cb93e041c6/viruses-15-02134-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/b8bbd2325eea/viruses-15-02134-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/4ff6574eb63e/viruses-15-02134-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/dcb86e6b16c9/viruses-15-02134-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/10612027/09bca1312456/viruses-15-02134-g008.jpg

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