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  • 1
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    Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-19
    Description: Latency and ongoing replication have both been proposed to explain the drug-insensitive human immunodeficiency virus (HIV) reservoir maintained during antiretroviral therapy. Here we explore a novel mechanism for ongoing HIV replication in the face of antiretroviral drugs. We propose a model whereby multiple infections per cell lead to reduced sensitivity to drugs without requiring drug-resistant mutations, and experimentally validate the model using multiple infections per cell by cell-free HIV in the presence of the drug tenofovir. We then examine the drug sensitivity of cell-to-cell spread of HIV, a mode of HIV transmission that can lead to multiple infection events per target cell. Infections originating from cell-free virus decrease strongly in the presence of antiretrovirals tenofovir and efavirenz whereas infections involving cell-to-cell spread are markedly less sensitive to the drugs. The reduction in sensitivity is sufficient to keep multiple rounds of infection from terminating in the presence of drugs. We examine replication from cell-to-cell spread in the presence of clinical drug concentrations using a stochastic infection model and find that replication is intermittent, without substantial accumulation of mutations. If cell-to-cell spread has the same properties in vivo, it may have adverse consequences for the immune system, lead to therapy failure in individuals with risk factors, and potentially contribute to viral persistence and hence be a barrier to curing HIV infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sigal, Alex -- Kim, Jocelyn T -- Balazs, Alejandro B -- Dekel, Erez -- Mayo, Avi -- Milo, Ron -- Baltimore, David -- HHSN266200500035C/PHS HHS/ -- T32 AI089398/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Aug 17;477(7362):95-8. doi: 10.1038/nature10347.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, California 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21849975" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/analogs & derivatives/pharmacology ; Anti-Retroviral Agents/*pharmacology ; Cell Line ; Drug Resistance, Viral/physiology ; HEK293 Cells ; HIV Infections/transmission/*virology ; HIV-1/drug effects/*physiology ; Humans ; Models, Biological ; Organophosphonates/pharmacology ; Tenofovir ; Virus Replication/drug effects/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Mutational inactivation of STAG2 causes aneuploidy in human cancer (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: Most cancer cells are characterized by aneuploidy, an abnormal number of chromosomes. We have identified a clue to the mechanistic origins of aneuploidy through integrative genomic analyses of human tumors. A diverse range of tumor types were found to harbor deletions or inactivating mutations of STAG2, a gene encoding a subunit of the cohesin complex, which regulates the separation of sister chromatids during cell division. Because STAG2 is on the X chromosome, its inactivation requires only a single mutational event. Studying a near-diploid human cell line with a stable karyotype, we found that targeted inactivation of STAG2 led to chromatid cohesion defects and aneuploidy, whereas in two aneuploid human glioblastoma cell lines, targeted correction of the endogenous mutant alleles of STAG2 led to enhanced chromosomal stability. Thus, genetic disruption of cohesin is a cause of aneuploidy in human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3374335/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3374335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solomon, David A -- Kim, Taeyeon -- Diaz-Martinez, Laura A -- Fair, Joshlean -- Elkahloun, Abdel G -- Harris, Brent T -- Toretsky, Jeffrey A -- Rosenberg, Steven A -- Shukla, Neerav -- Ladanyi, Marc -- Samuels, Yardena -- James, C David -- Yu, Hongtao -- Kim, Jung-Sik -- Waldman, Todd -- CA097257/CA/NCI NIH HHS/ -- R01 CA133662/CA/NCI NIH HHS/ -- R01 CA138212/CA/NCI NIH HHS/ -- R01 CA169345/CA/NCI NIH HHS/ -- R01CA115699/CA/NCI NIH HHS/ -- R21CA143282/CA/NCI NIH HHS/ -- Z01 HG200337-01/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):1039-43. doi: 10.1126/science.1203619.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852505" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Antigens, Nuclear/*genetics/*physiology ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; Chromatids/physiology ; *Chromosomal Instability ; Chromosomes, Human, X/genetics ; Female ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Gene Targeting ; Glioblastoma/*genetics ; Humans ; Karyotyping ; Male ; Melanoma/genetics ; Mutation ; Neoplasms/*genetics ; Polymorphism, Single Nucleotide ; Sarcoma, Ewing/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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