来自用户 龙海晨 的文献。
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41.
龙海晨
(2022-03-31 12:25):
#paper doi: 10.1186/s12935-022-02506-0 Cancer Cell International (2022) 22:94 HPV16 E6 gene polymorphisms
and the functions of the mutation site
in cervical cancer among Uygur ethnic and Han
nationality women in Xinjiang, China
三月比较忙，用自己课题组的文献发过来应该也符合要求吧，用生物信息学技术和细胞生物学，分子生物学实验。文章探寻维吾尔族和汉族妇女感染HPV的基因型分布。分析高危型病毒HPV16E6基因多态性位点及其与宫颈癌发生发展的关系。使用欧洲标准原型对HPV16 E6序列进行进化树分析，PV16 E6-T295/T350、G295/G350和T295/G350 GV230载体稳定转染宫颈癌C33A细胞，通过CCK8和克隆形成试验、转移膨胀和细胞划痕试验、流式细胞仪试验分析细胞增殖、迁移和侵袭、凋亡。
研究结果：1. 2879人中HPV总感染率为26.390%（760/2879），维吾尔族为22.87%（196/857），汉族为27.89%（564/2022）（P<0.05）。
2.在110个突变中，65例E6基因在核苷酸350（T350G）处发生突变亮氨酸变成缬氨酸（L83V）。此外，还有7例E6基因在295核苷酸处发生突变（T295G），天冬氨酸转变为谷氨酸（D64E）。
3.当突变位点的E6载体被转染到C33A中时，它们能促进细胞增殖、迁移、侵袭，并抑制细胞凋亡。T295/G350-E6为阳性显著强于G295/G350和T295/T350，G295/G350显著强于T295/T350（P<0.05）。T295/G350对C33A细胞的作用最强，G295/G350明显强于T295/T350（P<0.05）。
结论：1.中国新疆维吾尔族和汉族的HPV阳性感染率不同，感染的基因型分布也不同。
2.用不同的真核表达载体转染C33A细胞后，
T295/G350比G295/G350突变位点在更大程度上促进了C33A细胞的增殖、迁移和侵袭，G295/G350比T295/T350有更强的效果。
IF:5.300Q1
Cancer cell international,
2022-Feb-22.
DOI: 10.1186/s12935-022-02506-0
PMID: 35193568
PMCID:PMC8862000
Abstract:
BACKGROUND: To investigate the genotype distribution of human papillomavirus (HPV) in infected Uygur and Han women in Xinjiang, China; analyze the HPV16 E6 gene polymorphism site and relationship with the …
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BACKGROUND: To investigate the genotype distribution of human papillomavirus (HPV) in infected Uygur and Han women in Xinjiang, China; analyze the HPV16 E6 gene polymorphism site and relationship with the development of cervical cancer.METHODS: The HPV16 E6 sequence was analyzed using the European standard prototype to perform an evolutionary tree. HPV16 E6-T295/T350, G295/G350, and T295/G350 GV230 vectors were stably transfected into cervical cancer C33A cells to analyze the cell proliferation, migration and invasion, apoptosis by CCK8 and clonogenic assays, transwell and cell scratch assays, FACS experiments.RESULTS: The total HPV infection rate was 26.390% (760/2879), whereas the Uygur 22.87% (196/857) and the Han was 27.89% (564/2022) (P < 0.05). Among 110 mutations, 65 cases of E6 genes were mutated at nucleotide 350 (T350G) with the leucine changing to valine (L83V). Moreover, there were 7 cases of E6 gene mutated at nucleotide 295 (T295G) with aspartic changing to glutamic (D64E). When E6 vector(s) of mutations sites were transfected into C33A cells, they were found to promote cellular proliferation, migration, invasion, and inhibit apoptosis. T295/G350-E6 was significantly stronger than G295/G350 and T295/T350, G295/G350 was significantly stronger than T295/T350 (P < 0.05). The T295/G350 had the strongest effect on C33A cells and G295/G350 was significantly stronger than T295/T350 (P < 0.05).CONCLUSIONS: The positive HPV infection rates differed between the Uygur and Han in Xinjiang, China, and the genotype distribution of infection was different. After transfecting C33A cells with different eukaryotic expression vectors, the T295/G350 mutation site promoted the proliferation, migration, and invasion of C33A cells to a greater extent than G295/G350; however, G295/G350 had a stronger effect than T295/T350.
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42.
龙海晨
(2022-02-16 00:55):
#paper doi:10.1126/science.aah5869 Science, 2016, Generation of influenza A viruses as live but replication-incompetent virus vaccines
。推荐理由。”通过反向遗传学设计研制甲型流感病毒疫苗的论文。研究解决的问题：
1.可以快速大量生产活病毒疫苗（RNA）
2.信使RNA中引入了一个终止密码子让病毒失去复制能力（与之前的方法相比便宜高效）
3.插入位置在保守区，病毒若通过突变的形式恢复制能力会直接死亡
4.技术的核心：拥有用于病毒恢复复制能力的细胞系用于生产病毒，作为疫苗。病毒离开专门细胞系后丧失复制能力。
5.意外的收获：可以当治疗药物使用。新的病毒和野生型结合会使野生型病毒消失。（之前的技术常发生：活疫苗病毒与野生病毒相遇结果活疫苗产生毒性）。通过在（甲型）流感病毒的信使RNA中引入了一个终止密码子，并保留病毒的完整结构。这样，保留了感染性的病毒进入人体后，可以激活人体细胞的全部免疫反应，但由于终止密码子的存在，病毒无法进行蛋白质翻译，因而失去复制能力。
Science (New York, N.Y.),
2016-12-02.
PMID: 27934767
Abstract:
The conversion of life-threatening viruses into live but avirulent vaccines represents a revolution in vaccinology. In a proof-of-principle study, we expanded the genetic code of the genome of influenza A …
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The conversion of life-threatening viruses into live but avirulent vaccines represents a revolution in vaccinology. In a proof-of-principle study, we expanded the genetic code of the genome of influenza A virus via a transgenic cell line containing orthogonal translation machinery. This generated premature termination codon (PTC)-harboring viruses that exerted full infectivity but were replication-incompetent in conventional cells. Genome-wide optimization of the sites for incorporation of multiple PTCs resulted in highly reproductive and genetically stable progeny viruses in transgenic cells. In mouse, ferret, and guinea pig models, vaccination with PTC viruses elicited robust humoral, mucosal, and T cell-mediated immunity against antigenically distinct influenza viruses and even neutralized existing infecting strains. The methods presented here may become a general approach for generating live virus vaccines that can be adapted to almost any virus.
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