Retrovirology最新文献

{"title":"Replication-competent HIV-1 in human alveolar macrophages and monocytes despite nucleotide pools with elevated dUTP.","authors":"Junru Cui,&nbsp;Mesfin Meshesha,&nbsp;Natela Churgulia,&nbsp;Christian Merlo,&nbsp;Edward Fuchs,&nbsp;Jennifer Breakey,&nbsp;Joyce Jones,&nbsp;James T Stivers","doi":"10.1186/s12977-022-00607-2","DOIUrl":"https://doi.org/10.1186/s12977-022-00607-2","url":null,"abstract":"<p><strong>Background: </strong>Although CD4⁺ memory T cells are considered the primary latent reservoir for HIV-1, replication competent HIV has been detected in tissue macrophages in both animal and human studies. During in vitro HIV infection, the depleted nucleotide pool and high dUTP levels in monocyte derived macrophages (MDM) leads to proviruses with high levels of dUMP, which has been implicated in viral restriction or reduced transcription depending on the uracil base excision repair (UBER) competence of the macrophage. Incorporated dUMP has also been detected in viral DNA from circulating monocytes (MC) and alveolar macrophages (AM) of HIV infected patients on antiretroviral therapy (ART), establishing the biological relevance of this phenotype but not the replicative capacity of dUMP-containing proviruses.</p><p><strong>Results: </strong>As compared to in vitro differentiated MDM, AM from normal donors had sixfold lower levels of dTTP and a sixfold increased dUTP/dTTP, indicating a highly restrictive dNTP pool for reverse transcription. Expression of uracil DNA glycosylase (UNG) was eightfold lower in AM compared to the already low levels in MDM. Accordingly, ~ 80% of HIV proviruses contained dUMP, which persisted for at least 14-days due to low UNG excision activity. Unlike MDM, AM expression levels of UNG and SAM and HD domain containing deoxynucleoside triphosphate triphosphohydrolase 1 (SAMHD1) increased over 14 days post-HIV infection, while dUTP nucleotidohydrolase (DUT) expression decreased. These AM-specific effects suggest a restriction response centered on excising uracil from viral DNA copies and increasing relative dUTP levels. Despite the restrictive nucleotide pools, we detected rare replication competent HIV in AM, peripheral MC, and CD4⁺ T cells from ART-treated donors.</p><p><strong>Conclusions: </strong>These findings indicate that the potential integration block of incorporated dUMP is not realized during in vivo infection of AM and MC due to the near absence of UBER activity. In addition, the increased expression of UNG and SAMHD1 in AM post-infection is too slow to prevent integration. Accordingly, dUMP persists in integrated viruses, which based on in vitro studies, can lead to transcriptional silencing. This possible silencing outcome of persistent dUMP could promote viral latency until the repressive effects of viral dUMP are reversed.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"21"},"PeriodicalIF":3.3,"publicationDate":"2022-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9482235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10383036","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}

{"title":"The KT Jeang Retrovirology prize 2022: Florence Margottin-Goguet.","authors":"","doi":"10.1186/s12977-022-00606-3","DOIUrl":"https://doi.org/10.1186/s12977-022-00606-3","url":null,"abstract":"","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"20"},"PeriodicalIF":3.3,"publicationDate":"2022-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9446835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10367592","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}

{"title":"An endogenous lentivirus in the germline of a rodent","authors":"R. Kambol, Anna Gatseva, R. Gifford","doi":"10.1101/2022.09.01.506243","DOIUrl":"https://doi.org/10.1101/2022.09.01.506243","url":null,"abstract":"Lentiviruses (genus Lentivirus ) are complex retroviruses that infect a broad range of mammals, including humans. Unlike many other retrovirus genera, lentiviruses have only rarely been incorporated into the mammalian germline. However, a small number of endogenous retrovirus (ERV) lineages have been identified, and these rare genomic “fossils” can provide crucial insights into the long-term history of lentivirus evolution. Here, we describe a previously unreported endogenous lentivirus lineage in the genome of the South African springhare ( Pedetes capensis ), demonstrating that the host range of lentiviruses has historically extended to rodents (order Rodentia). Furthermore, through comparative and phylogenetic analysis of lentivirus and ERV genomes, considering the biogeographic and ecological characteristics of host species, we reveal broader insights into the long-term evolutionary history of the genus.","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2022-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49610088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The key amino acid sites 199-205, 269, 319, 321 and 324 of ALV-K env contribute to the weaker replication capacity of ALV-K than ALV-A.","authors":"Jian Chen,&nbsp;Jinqun Li,&nbsp;Xinyi Dong,&nbsp;Ming Liao,&nbsp;Weisheng Cao","doi":"10.1186/s12977-022-00598-0","DOIUrl":"https://doi.org/10.1186/s12977-022-00598-0","url":null,"abstract":"<p><strong>Background: </strong>Avian leukosis virus (ALV) is an infectious retrovirus, that mainly causes various forms of tumours, immunosuppression, a decreased egg production rate and slow weight gain in poultry. ALV consists of 11 subgroups, A-K, among which ALV-K is an emerging subgroup that has become prevalent in the past 10 years. Most ALV-K isolates showed weak replication ability and pathogenicity. In this study, the weak replication ability of ALV-K was explored from the perspective of the interaction between ALV-K gp85 and the Tva receptor.</p><p><strong>Methods: </strong>Fourteen soluble recombinant ALV-A/K gp85 chimeric proteins were constructed by substituting the sequence difference regions (hr1, hr2 and vr3) of the ALV-A gp85 protein with the skeleton ALV-K gp85 protein for co-IP and competitive blocking tests.</p><p><strong>Results: </strong>The binding capacity of ALV-K gp85 to Tva was significantly weaker than that of ALV-A gp85 (P < 0.05) and the key amino acid sites 199-205, 269, 319, 321 and 324 of ALV-K env contributed to the weaker replication capacity of ALV-K than ALV-A.</p><p><strong>Conclusions: </strong>This is the first study to reveal the molecular factors of the weak replication ability of ALV-K from the perspective of the interaction of ALV-K gp85 to Tva, providing a basis for further elucidation of the infection mechanism of ALV-K.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"19"},"PeriodicalIF":3.3,"publicationDate":"2022-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9400301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10376932","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}

{"title":"Opposing roles of CLK SR kinases in controlling HIV-1 gene expression and latency.","authors":"Subha Dahal,&nbsp;Kiera Clayton,&nbsp;Terek Been,&nbsp;Raphaële Fernet-Brochu,&nbsp;Alonso Villasmil Ocando,&nbsp;Ahalya Balachandran,&nbsp;Mikaël Poirier,&nbsp;Rebecca Kaddis Maldonado,&nbsp;Lulzim Shkreta,&nbsp;Kayluz Frias Boligan,&nbsp;Furkan Guvenc,&nbsp;Fariha Rahman,&nbsp;Donald Branch,&nbsp;Brendan Bell,&nbsp;Benoit Chabot,&nbsp;Scott D Gray-Owen,&nbsp;Leslie J Parent,&nbsp;Alan Cochrane","doi":"10.1186/s12977-022-00605-4","DOIUrl":"https://doi.org/10.1186/s12977-022-00605-4","url":null,"abstract":"<p><strong>Background: </strong>The generation of over 69 spliced HIV-1 mRNAs from one primary transcript by alternative RNA splicing emphasizes the central role that RNA processing plays in HIV-1 replication. Control is mediated in part through the action of host SR proteins whose activity is regulated by multiple SR kinases (CLK1-4, SRPKs).</p><p><strong>Methods: </strong>Both shRNA depletion and small molecule inhibitors of host SR kinases were used in T cell lines and primary cells to evaluate the role of these factors in the regulation of HIV-1 gene expression. Effects on virus expression were assessed using western blotting, RT-qPCR, and immunofluorescence.</p><p><strong>Results: </strong>The studies demonstrate that SR kinases play distinct roles; depletion of CLK1 enhanced HIV-1 gene expression, reduction of CLK2 or SRPK1 suppressed it, whereas CLK3 depletion had a modest impact. The opposing effects of CLK1 vs. CLK2 depletion were due to action at distinct steps; reduction of CLK1 increased HIV-1 promoter activity while depletion of CLK2 affected steps after transcript initiation. Reduced CLK1 expression also enhanced the response to several latency reversing agents, in part, by increasing the frequency of responding cells, consistent with a role in regulating provirus latency. To determine whether small molecule modulation of SR kinase function could be used to control HIV-1 replication, we screened a GSK library of protein kinase inhibitors (PKIS) and identified several pyrazolo[1,5-b] pyridazine derivatives that suppress HIV-1 gene expression/replication with an EC₅₀ ~ 50 nM. The compounds suppressed HIV-1 protein and viral RNA accumulation with minimal impact on cell viability, inhibiting CLK1 and CLK2 but not CLK3 function, thereby selectively altering the abundance of individual CLK and SR proteins in cells.</p><p><strong>Conclusions: </strong>These findings demonstrate the unique roles played by individual SR kinases in regulating HIV-1 gene expression, validating the targeting of these functions to either enhance latency reversal, essential for \"Kick-and-Kill\" strategies, or to silence HIV protein expression for \"Block-and-Lock\" strategies.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"18"},"PeriodicalIF":3.3,"publicationDate":"2022-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9319973","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}

{"title":"CRISPR/Cas9 genome editing to create nonhuman primate models for studying stem cell therapies for HIV infection.","authors":"Jenna Kropp Schmidt, Matthew R Reynolds, Thaddeus G Golos, Igor I Slukvin","doi":"10.1186/s12977-022-00604-5","DOIUrl":"10.1186/s12977-022-00604-5","url":null,"abstract":"<p><p>Nonhuman primates (NHPs) are well-established basic and translational research models for human immunodeficiency virus (HIV) infections and pathophysiology, hematopoietic stem cell (HSC) transplantation, and assisted reproductive technologies. Recent advances in CRISPR/Cas9 gene editing technologies present opportunities to refine NHP HIV models for investigating genetic factors that affect HIV replication and designing cellular therapies that exploit genetic barriers to HIV infections, including engineering mutations into CCR5 and conferring resistance to HIV/simian immunodeficiency virus (SIV) infections. In this report, we provide an overview of recent advances and challenges in gene editing NHP embryos and discuss the value of genetically engineered animal models for developing novel stem cell-based therapies for curing HIV.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"17"},"PeriodicalIF":3.3,"publicationDate":"2022-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9363854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9276209","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}

{"title":"Two lymphoid cell lines potently silence unintegrated HIV-1 DNAs.","authors":"Franziska K Geis,&nbsp;Demetra P Kelenis,&nbsp;Stephen P Goff","doi":"10.1186/s12977-022-00602-7","DOIUrl":"https://doi.org/10.1186/s12977-022-00602-7","url":null,"abstract":"<p><p>Mammalian cells mount a variety of defense mechanisms against invading viruses to prevent or reduce infection. One such defense is the transcriptional silencing of incoming viral DNA, including the silencing of unintegrated retroviral DNA in most cells. Here, we report that the lymphoid cell lines K562 and Jurkat cells reveal a dramatically higher efficiency of silencing of viral expression from unintegrated HIV-1 DNAs as compared to HeLa cells. We found K562 cells in particular to exhibit an extreme silencing phenotype. Infection of K562 cells with a non-integrating viral vector encoding a green fluorescent protein reporter resulted in a striking decrease in the number of fluorescence-positive cells and in their mean fluorescence intensity as compared to integration-competent controls, even though the levels of viral DNA in the nucleus were equal or in the case of 2-LTR circles even higher. The silencing in K562 cells was functionally distinctive. Histones loaded on unintegrated HIV-1 DNA in K562 cells revealed high levels of the silencing mark H3K9 trimethylation and low levels of the active mark H3 acetylation, as detected in HeLa cells. But infection of K562 cells resulted in low H3K27 trimethylation levels on unintegrated viral DNA as compared to higher levels in HeLa cells, corresponding to low H3K27 trimethylation levels of silent host globin genes in K562 cells as compared to HeLa cells. Most surprisingly, treatment with the HDAC inhibitor trichostatin A, which led to a highly efficient relief of silencing in HeLa cells, only weakly relieved silencing in K562 cells. In summary, we found that the capacity for silencing viral DNAs differs between cell lines in its extent, and likely in its mechanism.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":" ","pages":"16"},"PeriodicalIF":3.3,"publicationDate":"2022-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9271240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40578716","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}

{"title":"Innate immune regulation in HIV latency models.","authors":"Rebecca M Olson,&nbsp;Germán Gornalusse,&nbsp;Leanne S Whitmore,&nbsp;Dan Newhouse,&nbsp;Jennifer Tisoncik-Go,&nbsp;Elise Smith,&nbsp;Christina Ochsenbauer,&nbsp;Florian Hladik,&nbsp;Michael Gale","doi":"10.1186/s12977-022-00599-z","DOIUrl":"https://doi.org/10.1186/s12977-022-00599-z","url":null,"abstract":"<p><strong>Background: </strong>Innate immunity and type 1 interferon (IFN) defenses are critical for early control of HIV infection within CD4 + T cells. Despite these defenses, some acutely infected cells silence viral transcription to become latently infected and form the HIV reservoir in vivo. Latently infected cells persist through antiretroviral therapy (ART) and are a major barrier to HIV cure. Here, we evaluated innate immunity and IFN responses in multiple T cell models of HIV latency, including established latent cell lines, Jurkat cells latently infected with a reporter virus, and a primary CD4 + T cell model of virologic suppression.</p><p><strong>Results: </strong>We found that while latently infected T cell lines have functional RNA sensing and IFN signaling pathways, they fail to induce specific interferon-stimulated genes (ISGs) in response to innate immune activation or type 1 IFN treatment. Jurkat cells latently infected with a fluorescent reporter HIV similarly demonstrate attenuated responses to type 1 IFN. Using bulk and single-cell RNA sequencing we applied a functional genomics approach and define ISG expression dynamics in latent HIV infection, including HIV-infected ART-suppressed primary CD4 + T cells.</p><p><strong>Conclusions: </strong>Our observations indicate that HIV latency and viral suppression each link with cell-intrinsic defects in specific ISG induction. We identify a set of ISGs for consideration as latency restriction factors whose expression and function could possibly mitigate establishing latent HIV infection.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"15"},"PeriodicalIF":3.3,"publicationDate":"2022-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9270781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10663112","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}

{"title":"Repression of HIV-1 reactivation mediated by CRISPR/dCas9-KRAB in lymphoid and myeloid cell models.","authors":"Lendel Correia da Costa,&nbsp;Larissa Maciel Bomfim,&nbsp;Uilla Victoria Torres Dittz,&nbsp;Camila de Almeida Velozo,&nbsp;Rodrigo Delvecchio da Cunha,&nbsp;Amilcar Tanuri","doi":"10.1186/s12977-022-00600-9","DOIUrl":"https://doi.org/10.1186/s12977-022-00600-9","url":null,"abstract":"<p><strong>Background: </strong>Despite antiretroviral treatment efficacy, it does not lead to the complete eradication of HIV infection. Consequently, reactivation of the virus from latently infected cell reservoirs is a major challenge toward cure efforts. Two strategies targeting viral latency are currently under investigation: the \"shock and kill\" and the \"block and lock.\" The \"Block and Lock\" methodology aims to control HIV-1 latency reactivation, promoting a functional cure. We utilized the CRISPR/dCas9-KRAB platform, which was initially developed to suppress cellular genes transcription, to block drug-induced HIV-1 reactivation in latently infected T cells and myeloid cells.</p><p><strong>Results: </strong>We identified a set of five sgRNAs targeting the HIV-1 proviral genome (LTR1-LTR5), having the lowest nominated off-target activity, and transduced them into the latently infected lymphoid (J-Lat 10.6) and myeloid (U1) cell lines. One of the sgRNAs (LTR5), which binds specifically in the HIV-1 LTR NFκB binding site, was able to promote robust repression of HIV-1 reactivation in latently infected T cells stimulated with Phorbol 12-Myristate 13-Acetate (PMA) and Ingenol B (IngB), both potent protein kinase C (PKC) stimulators. Reactivation with HDAC inhibitors, such as SAHA and Panobinostat, showed the same strong inhibition of reactivation. Additionally, we observed a hundred times reduction of HIV-1 RNA expression levels in the latently infected myeloid cell line, U1 induced with IngB.</p><p><strong>Conclusion: </strong>Taken together, our results show that the KRAB fused CRISPR/dCas9 system can robustly prevent the HIV-1 latency reactivation process, mediated by PMA or IngB and SAHA or Panobinostat, both in myeloid and lymphoid HIV-1 latently infected cells. In addition, we demonstrated that KRAB repressor protein is crucial to reactivation resistance phenotype, and we have identified some useful hotspots sequences in HIV-1 LTR for the design sgRNAs.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":" ","pages":"12"},"PeriodicalIF":3.3,"publicationDate":"2022-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9215058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40210164","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}

{"title":"Comprehensive identification and characterization of the HERV-K (HML-9) group in the human genome.","authors":"Lei Jia, Mengying Liu, Caiqin Yang, Hanping Li, Yongjian Liu, Jingwan Han, Xiuli Zhai, Xiaolin Wang, Tianyi Li, Jingyun Li, Bohan Zhang, Changyuan Yu, Lin Li","doi":"10.1186/s12977-022-00596-2","DOIUrl":"10.1186/s12977-022-00596-2","url":null,"abstract":"<p><strong>Background: </strong>Human endogenous retroviruses (HERVs) result from ancestral infections caused by exogenous retroviruses that became incorporated into the germline DNA and evolutionarily fixed in the human genome. HERVs can be transmitted vertically in a Mendelian fashion and be stably maintained in the human genome, of which they are estimated to comprise approximately 8%. HERV-K (HML1-10) transcription has been confirmed to be associated with a variety of diseases, such as breast cancer, lung cancer, prostate cancer, melanoma, rheumatoid arthritis, and amyotrophic lateral sclerosis. However, the poor characterization of HML-9 prevents a detailed understanding of the regulation of the expression of this family in humans and its impact on the host genome. In light of this, a precise and updated HERV-K HML-9 genomic map is urgently needed to better evaluate the role of these elements in human health.</p><p><strong>Results: </strong>We report a comprehensive analysis of the presence and distribution of HERV-K HML-9 elements within the human genome, with a detailed characterization of the structural and phylogenetic properties of the group. A total of 23 proviruses and 47 solo LTR elements were characterized, with a detailed description of the provirus structure, integration time, potential regulated genes, transcription factor binding sites (TFBS), and primer binding site (PBS) features. The integration time results showed that the HML-9 elements found in the human genome integrated into the primate lineage between 17.5 and 48.5 million years ago (mya).</p><p><strong>Conclusion: </strong>The results provide a clear characterization of HML-9 and a comprehensive background for subsequent functional studies.</p>","PeriodicalId":21123,"journal":{"name":"Retrovirology","volume":"19 1","pages":"11"},"PeriodicalIF":2.7,"publicationDate":"2022-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9178832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65721241","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}