Retrovirology最新文献_第10页

Abstract withdrawn 摘要已撤回

IF 3.3 3区医学

Retrovirology Pub Date : 2019-09-01 DOI: 10.1186/1742-4690-2-S1-S131

R. Castillo, Ngo Quy Chau, Vu Van Giap, L. Hoan, C. Wong

引用次数: 0

The KT Jeang Prize 2019: Reuben S. Harris 2019年KT Jeang奖:鲁本·s·哈里斯

IF 3.3 3区医学

Retrovirology Pub Date : 2019-08-29 DOI: 10.1186/s12977-019-0486-x

Retrovirology Editorial

引用次数: 0

Impact of host immunity on HTLV-1 pathogenesis: potential of Tax-targeted immunotherapy against ATL 宿主免疫对HTLV-1发病机制的影响:税收靶向免疫治疗ATL的潜力

IF 3.3 3区医学

Retrovirology Pub Date : 2019-08-22 DOI: 10.1186/s12977-019-0484-z

M. Kannagi, A. Hasegawa, Yoshiko Nagano, Shuichi Kimpara, Y. Suehiro

引用次数: 33

A trip down memory lane with Retrovirology 逆转录病毒学的记忆之旅

IF 3.3 3区医学

Retrovirology Pub Date : 2019-08-21 DOI: 10.1186/s12977-019-0485-y

M. Benkirane, B. Berkhout, P. Borrow, A. Fassati, Masahiro Fujii, J. Garcia-Martinez, D. Margolis, M. Nijhuis, Leslie Parent, K. Strebel, François Venter, F. Kirchhoff, Andrew Lever, Susan R Ross, Johnson Mak

引用次数: 0

Comparative virology of HTLV-1 and HTLV-2 HTLV-1和HTLV-2的比较病毒学

IF 3.3 3区医学

Retrovirology Pub Date : 2019-08-07 DOI: 10.1186/s12977-019-0483-0

Michael P Martinez, Jacob Al-Saleem, P. Green

引用次数: 57

Correction to: CCR5 editing by Staphylococcus aureus Cas9 in human primary CD4+ T cells and hematopoietic stem/progenitor cells promotes HIV-1 resistance and CD4+ T cell enrichment in humanized mice 更正:金黄色葡萄球菌Cas9在人原代CD4+ T细胞和造血干细胞/祖细胞中编辑CCR5可促进人源化小鼠对HIV-1的抵抗和CD4+ T细胞的富集

IF 3.3 3区医学

Retrovirology Pub Date : 2019-07-23 DOI: 10.1186/s12977-019-0482-1

Qiao Xiao, Shuliang Chen, Qiankun Wang, Zhepeng Liu, Shuai Liu, Huan Deng, W. Hou, Dongcheng Wu, Yong Xiong, Jiafu Li, D. Guo

引用次数: 1

Sequential trafficking of Env and Gag to HIV-1 T cell virological synapses revealed by live imaging. 实时成像揭示了Env和Gag在HIV-1 T细胞病毒学突触上的顺序运输。

IF 3.3 3区医学

Retrovirology Pub Date : 2019-01-15 DOI: 10.1186/s12977-019-0464-3

Lili Wang, Sudeh Izadmehr, Edwin Kamau, Xiang-Peng Kong, Benjamin K Chen

{"title":"Sequential trafficking of Env and Gag to HIV-1 T cell virological synapses revealed by live imaging.","authors":"Lili Wang, Sudeh Izadmehr, Edwin Kamau, Xiang-Peng Kong, Benjamin K Chen","doi":"10.1186/s12977-019-0464-3","DOIUrl":"https://doi.org/10.1186/s12977-019-0464-3","url":null,"abstract":"Background: HIV infection is enhanced by cell adhesions that form between infected and uninfected T cells called virological synapses (VS). VS are initiated by an interaction between Env and CD4 on cell surfaces and result in the recruitment of virus assembly to the site of cell-cell contact. However, the recruitment of Env to the VS and its relationship to Gag recruitment is not well defined.Results: To study the trafficking of HIV-1 Env through the VS, we constructed a molecular clone of HIV carrying a green fluorescent protein-Env fusion protein called, HIV Env-isfGFP-∆V1V2. The Env-isfGFP-∆V1V2 fusion protein does not produce virus particles on its own, but can be rescued by cotransfection with full-length HIV constructs and produce virus particles that package the fluorescent Env. These rescued fluorescent Env can participate in VS formation and can be used to directly image CD4-dependent Env transfer across VS from donor to target cells. The movements of fluorescently tagged Gag and Env to the VS and transfer into target cells can be also tracked through live imaging. Time lapse live imaging reveals evidence of limited Env accumulation at the site of cell-cell contact shortly after cell adhesion, followed by Gag re-distribution to contact area. Both Gag and Env can be recruited to form button-like spots characteristic of VS.Conclusions: Env and Gag are recruited to the VS in a coordinated temporal sequence and subsequently transfer together across the synapse into the target cell. Env accumulations, when observed, are earlier than Gag re-distribution to the contact area during formation of VS.","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"16 1","pages":"2"},"PeriodicalIF":3.3,"publicationDate":"2019-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s12977-019-0464-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10415652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 21

The expanding array of HIV broadly neutralizing antibodies. 不断扩大的艾滋病毒抗体广泛中和。

IF 3.3 3区医学

Retrovirology Pub Date : 2018-10-16 DOI: 10.1186/s12977-018-0453-y

Laura E McCoy

{"title":"The expanding array of HIV broadly neutralizing antibodies.","authors":"Laura E McCoy","doi":"10.1186/s12977-018-0453-y","DOIUrl":"https://doi.org/10.1186/s12977-018-0453-y","url":null,"abstract":"A large array of broadly neutralizing antibodies (bnAbs) against HIV have been isolated and described, particularly in the last decade. This continually expanding array of bnAbs has crucially led to the identification of novel epitopes on the HIV envelope protein via which antibodies can block a broad range of HIV strains. Moreover, these studies have produced high-resolution understanding of these sites of vulnerability on the envelope protein. They have also clarified the mechanisms of action of bnAbs and provided detailed descriptions of B cell ontogenies from which they arise. However, it is still not possible to predict which HIV-infected individuals will go onto develop breath nor is it possible to induce neutralization breadth by immunization in humans. This review aims to discuss the major insights gained so far and also to evaluate the requirement to continue isolating and characterizing new bnAbs. While new epitopes may remain to be uncovered, a clearer probable benefit of further bnAb characterization is a greater understanding of key decision points in bnAb development within the anti-HIV immune response. This in turn may lead to new insights into how to trigger bnAbs by immunization and more clearly define the challenges to using bnAbs as therapeutic agents.","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"15 1","pages":"70"},"PeriodicalIF":3.3,"publicationDate":"2018-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s12977-018-0453-y","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10001349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 39

Abstract withdrawn 抽象撤销

IF 3.3 3区医学

Retrovirology Pub Date : 2018-10-01 DOI: 10.1186/1742-4690-2-S1-P136

引用次数: 0

A CRISPR screen for factors regulating SAMHD1 degradation identifies IFITMs as potent inhibitors of lentiviral particle delivery. 通过CRISPR筛选SAMHD1降解调节因子，发现IFITMs是慢病毒颗粒递送的有效抑制剂。

IF 3.3 3区医学

Retrovirology Pub Date : 2018-03-20 DOI: 10.1186/s12977-018-0409-2

Ferdinand Roesch, Molly OhAinle, Michael Emerman

{"title":"A CRISPR screen for factors regulating SAMHD1 degradation identifies IFITMs as potent inhibitors of lentiviral particle delivery.","authors":"Ferdinand Roesch, Molly OhAinle, Michael Emerman","doi":"10.1186/s12977-018-0409-2","DOIUrl":"https://doi.org/10.1186/s12977-018-0409-2","url":null,"abstract":"The InterFeron Induced TransMembrane (IFITM) proteins are interferon stimulated genes that restrict many viruses, including HIV-1. SAMHD1 is another restriction factor blocking replication of HIV-1 and other viruses. Some lentiviruses evolved Vpx/Vpr proteins to degrade SAMHD1. However, this viral antagonism can be perturbed by host mechanisms: a recent study showed that in interferon (IFN) treated THP1 cells, Vpx is unable to degrade SAMHD1. In the present work, we designed an Interferon Stimulated Genes (ISGs)-targeted CRISPR knockout screen in order to identify ISGs regulating this phenotype. We found that IFITM proteins contribute to the IFNα-mediated protection of SAMHD1 by blocking VSV-G-mediated entry of the lentiviral particles delivering Vpx. Consistent with this, IFNα treatment and IFITM expression had no effect when the A-MLV envelope was used for pseudotyping. Using an assay measuring viral entry, we show that IFNα and IFITMs directly block the delivery of Vpx into cells by inhibiting VSV-G viral fusion. Strikingly, the VSV-G envelope was significantly more sensitive to this IFNα entry block and to IFITMs than HIV-1's natural envelope. This highlights important differences between VSV-G pseudotyped and wild-type HIV-1, in particular relative to the pathways they use for viral entry, suggesting that HIV-1 may have evolved to escape restriction factors blocking entry.","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"15 1","pages":"26"},"PeriodicalIF":3.3,"publicationDate":"2018-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s12977-018-0409-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9989470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 18