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  • 1
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    Contribution of human alpha-defensin 1, 2, and 3 to the anti-HIV-1 activity of CD8 antiviral factor (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-09-28
    Description: It has been known since 1986 that CD8 T lymphocytes from certain HIV-1-infected individuals who are immunologically stable secrete a soluble factor, termed CAF, that suppresses HIV-1 replication. However, the identity of CAF remained elusive despite an extensive search. By means of a protein-chip technology, we identified a cluster of proteins that were secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated. These proteins were identified as alpha-defensin 1, 2, and 3 on the basis of specific antibody recognition and amino acid sequencing. CAF activity was eliminated or neutralized by an antibody specific for human alpha-defensins. Synthetic and purified preparations of alpha-defensins also inhibited the replication of HIV-1 isolates in vitro. Taken together, our results indicate that alpha-defensin 1, 2, and 3 collectively account for much of the anti-HIV-1 activity of CAF that is not attributable to beta-chemokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Linqi -- Yu, Wenjie -- He, Tian -- Yu, Jian -- Caffrey, Rebecca E -- Dalmasso, Enrique A -- Fu, Siyu -- Pham, Thang -- Mei, Jianfeng -- Ho, Jaclyn J -- Zhang, Wenyong -- Lopez, Peter -- Ho, David D -- AI-42848/AI/NIAID NIH HHS/ -- M01-RR00102/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 1;298(5595):995-1000. Epub 2002 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, The Rockefeller University, 455 First Avenue, New York, NY 10016, USA. lzhang@adarc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12351674" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Monoclonal ; Antiviral Agents/chemistry/isolation & purification/*pharmacology ; CD8-Positive T-Lymphocytes/chemistry/*immunology ; Cells, Cultured ; Chemokines, CC/immunology/physiology ; HIV Infections/*immunology/virology ; HIV Long-Term Survivors ; HIV-1/drug effects/*physiology ; Humans ; Mass Spectrometry ; Molecular Sequence Data ; Neutrophils/chemistry/immunology ; Protein Array Analysis ; Virus Replication ; alpha-Defensins/chemistry/isolation & purification/pharmacology/*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)
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  • 2
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    Functional interaction and partial homology between human immunodeficiency virus and neuroleukin (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: Dementia is common in patients with AIDS, but the mechanism by which the human immunodeficiency virus type 1 (HIV-1) causes the neurological impairment is unknown. In this study the possibility that an antigen of HIV-1 suppresses neuronal responses to neurotrophic factors was examined. Both HIV-1 and a related retrovirus, simian immunodeficiency virus (SIV), inhibited the growth of sensory neurons from chick dorsal root ganglia in medium containing neuroleukin (NLK) but not in medium containing nerve growth factor. An unrelated type D retrovirus, simian acquired immunodeficiency syndrome virus, did not affect the growth of neurons in the presence of either neurotrophic factor. The inhibition by HIV-1 of neuron growth in the presence of NLK was found to be due to the gp120 envelope glycoprotein. Regions of sequence homology between gp120 and NLK may account for this inhibitory property of gp120 and functional interactions between gp120 and NLK may be important in the pathogenesis of the AIDS dementia complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, M R -- Ho, D D -- Gurney, M E -- 5P01 NS-21443/NS/NINDS NIH HHS/ -- K08-AI00685/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1047-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039662" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Brain/microbiology ; Cells, Cultured ; Ganglia, Spinal/drug effects ; Glucose-6-Phosphate Isomerase ; Growth Substances/*genetics/pharmacology ; HIV/*genetics ; HIV Envelope Protein gp120 ; Humans ; Lymphokines/*genetics/pharmacology ; Nerve Growth Factors/pharmacology ; Neurons, Afferent/drug effects ; Retroviridae Proteins/genetics/pharmacology ; Sequence Homology, Nucleic Acid ; Viral Envelope Proteins/genetics/pharmacology
    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
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    PAPER CURRENT
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