ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Human LilrB2 is a beta-amyloid receptor and its murine homolog PirB regulates synaptic plasticity in an Alzheimer's model (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-21
    Description: Soluble beta-amyloid (Abeta) oligomers impair synaptic plasticity and cause synaptic loss associated with Alzheimer's disease (AD). We report that murine PirB (paired immunoglobulin-like receptor B) and its human ortholog LilrB2 (leukocyte immunoglobulin-like receptor B2), present in human brain, are receptors for Abeta oligomers, with nanomolar affinity. The first two extracellular immunoglobulin (Ig) domains of PirB and LilrB2 mediate this interaction, leading to enhanced cofilin signaling, also seen in human AD brains. In mice, the deleterious effect of Abeta oligomers on hippocampal long-term potentiation required PirB, and in a transgenic model of AD, PirB not only contributed to memory deficits present in adult mice, but also mediated loss of synaptic plasticity in juvenile visual cortex. These findings imply that LilrB2 contributes to human AD neuropathology and suggest therapeutic uses of blocking LilrB2 function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853120/" 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/PMC3853120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Taeho -- Vidal, George S -- Djurisic, Maja -- William, Christopher M -- Birnbaum, Michael E -- Garcia, K Christopher -- Hyman, Bradley T -- Shatz, Carla J -- 5P50AG005134/AG/NIA NIH HHS/ -- 5R01AG041507/AG/NIA NIH HHS/ -- 5T32EY020485/EY/NEI NIH HHS/ -- EY02858/EY/NEI NIH HHS/ -- K08 NS069811/NS/NINDS NIH HHS/ -- K08NS069811/NS/NINDS NIH HHS/ -- NS069375/NS/NINDS NIH HHS/ -- R01 AG041507/AG/NIA NIH HHS/ -- R01 EY002858/EY/NEI NIH HHS/ -- R01 MH071666/MH/NIMH NIH HHS/ -- T32 EY020485/EY/NEI NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 20;341(6152):1399-404. doi: 10.1126/science.1242077.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Bio-X, James H. Clark Center, Stanford University, Stanford, CA 94305, USA. tkim808@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24052308" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*physiopathology ; Amyloid beta-Peptides/*metabolism/pharmacology ; Animals ; Disease Models, Animal ; Female ; HEK293 Cells ; Hippocampus/physiopathology ; Humans ; Long-Term Potentiation ; Male ; Membrane Glycoproteins/genetics/*physiology ; Mice ; Mice, Transgenic ; *Neuronal Plasticity ; Peptide Fragments/*metabolism/pharmacology ; Receptors, Immunologic/genetics/*physiology ; Synapses/*physiology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...