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  • 1
    Publication Date: 1984-08-31
    Description: A T lymphotropic virus found in patients with the acquired immune deficiency syndrome (AIDS) or lymphadenopathy syndrome has been postulated to be the cause of AIDS. Immunological analysis of this retrovirus and its biological properties suggest that it is a member of the family of human T-lymphotropic retroviruses known as HTLV. Accordingly, it has been named HTLV-III. In the present report it is shown by nucleic acid hybridization that sequences of the genome of HTLV-III are homologous to the structural genes (gag, pol, and env) of both HTLV-I and HTLV-II and to a potential coding region called pX located between the env gene and the long terminal repeating sequence that is unique to the HTLV family of retroviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arya, S K -- Gallo, R C -- Hahn, B H -- Shaw, G M -- Popovic, M -- Salahuddin, S Z -- Wong-Staal, F -- New York, N.Y. -- Science. 1984 Aug 31;225(4665):927-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089333" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Base Sequence ; Cloning, Molecular ; Dna ; DNA, Viral ; Deltaretrovirus/classification/*genetics ; Genes ; *Genes, Viral ; Humans ; *Nucleic Acid Hybridization ; RNA, Viral ; Repetitive Sequences, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1984-12-07
    Description: The human T-cell leukemia (lymphotropic) virus type III (HTLV-III) appears to be central to the causation of the acquired immune deficiency syndrome (AIDS). Two full-length integrated proviral DNA forms of HTLV-III have now been cloned and analyzed, and DNA sequences of the virus in cell lines and fresh tissues from patients with AIDS or AIDS-related complex (ARC) have been characterized. The results revealed that (i) HTLV-III is an exogenous human retrovirus, approximately 10 kilobases in length, that lacks nucleic acid sequences derived from normal human DNA; (ii) HTLV-III, unlike HTLV types I and II, shows substantial diversity in its genomic restriction enzyme cleavage pattern; (iii) HTLV-III persists in substantial amounts in cells as unintegrated linear DNA, an uncommon property that has been linked to the cytopathic effects of certain animal retroviruses; and (iv) HTLV-III viral DNA can be detected in low levels in fresh (primary) lymphoid tissue of a minority of patients with AIDS or ARC but appears not to be present in Kaposi's sarcoma tissue. These findings have important implications concerning the biological properties of HTLV-III and the pathophysiology of AIDS and Kaposi's sarcoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaw, G M -- Hahn, B H -- Arya, S K -- Groopman, J E -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1165-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095449" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Base Sequence ; Cell Line ; Child ; Cloning, Molecular ; Cytopathogenic Effect, Viral ; DNA Restriction Enzymes/metabolism ; DNA, Viral/*analysis ; Deltaretrovirus/*genetics ; Humans ; Male ; Nucleic Acid Hybridization
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1984-01-13
    Description: T-cell growth factor (TCGF) or interleukin-2 (IL-2), an immunoregulatory lymphokine, is produced by lectin- or antigen-activated mature T lymphocytes and in a constitutive manner by certain T-cell lymphoma cell lines. By means of a molecular clone of human TCGF and DNA extracted from a panel of somatic cell hybrids (rodent cells X normal human lymphocytes), the TCGF structural gene was identified on human chromosome 4. In situ hybridization of the TCGF clone to human chromosomes resulted in significant labeling of the midportion of the long arm of chromosome 4, indicating that the TCGF gene was located at band q26-28. Genomic DNA from a panel of hybrids prepared with HUT-102 B2 cells was examined with the same molecular clone. In this clone of cells, which produces human T-cell leukemia virus, the TCGF gene was also located on chromosome 4 and was apparently not rearranged. The homologous TCGF locus in the domestic cat was assigned to chromosome B1 by using a somatic cell hybrid panel that segregates cat chromosomes. Linkage studies as well as high-resolution G-trypsin banding indicate that this feline chromosome is partially homologous to human chromosome 4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seigel, L J -- Harper, M E -- Wong-Staal, F -- Gallo, R C -- Nash, W G -- O'Brien, S J -- New York, N.Y. -- Science. 1984 Jan 13;223(4632):175-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318318" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats/*genetics ; Chromosome Banding ; Chromosome Mapping ; *Chromosomes ; *Chromosomes, Human, 4-5 ; Cloning, Molecular ; Deltaretrovirus ; *Genes ; Genetic Linkage ; Humans ; Hybrid Cells ; Interleukin-2/*genetics ; Nucleic Acid Hybridization
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1988-07-15
    Description: In a study of the immunologic significance of the genetic diversity present within single isolates of human immunodeficiency virus type 1 (HIV-1), the neutralization of viruses derived from molecular clones of the HIV-1 strain HTLV-IIIB by an extensive panel of sera was compared. Sera from HIV-1-infected patients and from goats immunized with polyacrylamide gel-purified HIV-1 envelope glycoprotein (gp120), native gp120, or gp120-derived recombinant peptides, showed marked heterogeneity in neutralizing activity against these closely related viruses. The change of a single amino acid residue in gp120 may account for such "clonal restriction" of neutralizing activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Looney, D J -- Fisher, A G -- Putney, S D -- Rusche, J R -- Redfield, R R -- Burke, D S -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):357-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Viral Diseases, Walter Reed Army Institute of Research, Washington, DC 20307.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3388046" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Viral/*immunology ; Binding, Competitive ; Cloning, Molecular ; HIV/genetics/*immunology ; HIV Seropositivity/immunology ; Humans ; Molecular Sequence Data ; Neutralization Tests ; Oligopeptides/chemical synthesis/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 1985-04-05
    Description: Human T-cell lymphotropic virus type III (HTLV-III), the causative agent of the acquired immune deficiency syndrome (AIDS), was recently isolated and its genomic structure analyzed by DNA cloning methods. In the studies reported here a combined cloning and expression system was used to identify HTLV-III encoded peptides that react immunologically with antibodies in sera from AIDS patients. Cloned HTLV-III DNA was sheared into approximately 500-base-pair fragments and inserted into an "open reading frame" expression vector, pMR100. The inserted DNA was expressed in Escherichia coli transformants as a polypeptide fused to the lambda CI protein at its amino terminus and to beta-galactosidase at its carboxyl terminus. Sera from AIDS patients containing antibodies to HTLV-III were then used to screen for immunoreactive fusion proteins. Twenty clones, each specifying a fusion protein strongly reactive with AIDS serum, were identified. DNA sequence analysis indicated that the HTLV-III fragments were derived from the open reading frame DNA segments corresponding to the gag and pol gene coding regions and also the large open reading frame region (env-lor) located near the 3' end of the viral genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, N T -- Chanda, P K -- Barone, A D -- McKinney, S -- Rhodes, D P -- Tam, S H -- Shearman, C W -- Huang, J -- Chang, T W -- Gallo, R C -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):93-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2983429" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; Antibodies, Viral/immunology ; Cloning, Molecular ; DNA, Recombinant/metabolism ; DNA, Viral/genetics ; Deltaretrovirus/*genetics ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli/genetics ; Genes, Viral ; Genetic Vectors ; Humans ; Viral Proteins/*genetics/immunology/isolation & purification ; beta-Galactosidase/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1986-08-08
    Description: A variant of human T-lymphotropic virus type III (HTLV-III) is described that replicates but does not kill normal human T cells in vitro. This variant, designated X10-1, was derived from the genome of a cytopathic HTLV-III clone (pHXB2D) by excision of a 200-base pair segment in the 3' region of the virus, spanning the env and 3'-orf genes. Comparable variants with 55 to 109 base pairs deleted exclusively in 3'-orf produced, in contrast, virus that was extremely cytopathic. On the basis of these findings it is concluded that the 3'-orf gene is not required for cytopathogenicity or replication of HTLV-III. In addition, the results suggest that virus replication and cytotoxicity are not intrinsically coupled. Furthermore, since clone X10-1 retains the ability to trans-activate genes linked to the viral long terminal repeats, trans-activation per se is not responsible for T-cell killing by HTLV-III. These results also raise the possibility that the carboxyl terminus of the envelope gene of HTLV-III has a direct role in T-cell killing by this virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ratner, L -- Mitsuya, H -- Marselle, L M -- Harper, M E -- Broder, S -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):655-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3014663" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Cloning, Molecular ; Deltaretrovirus/*genetics/pathogenicity ; Humans ; Mutation ; Nucleic Acid Hybridization ; RNA, Viral/genetics ; T-Lymphocytes/microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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