Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q96DT5 (SIV)
 2,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhesus progenitor-enriched BM was exposed overnight to SIV and cultured in a limiting dilution assay where the potential for progenitor interaction with lymphocytes or macrophages was low. Virus was consistently isolated late in culture, detection being aided by coculture with CEM174 lymphoblasts. Although infected cells had reduced clonogenic activity, colonies were indistinguishable from those derived from uninfected BM with respect to proliferative potential, morphology, and longevity in culture. Primate immunodeficiency viruses, therefore, may infect immature BM populations, directly affecting hematopoietic activity.
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PMID:Recovery of the simian immunodeficiency virus (SIV) and depression of colony formation in in vitro infected progenitor cell-enriched rhesus bone marrow (BM). 194 3

We report here the results of molecular analysis of a simian immunodeficiency virus (designated SIVstm) which was isolated from a rhesus monkey inoculated with stored lymph node tissue of an Asian stump-tailed macaque. The latter monkey had died in 1977 during an epidemic of acquired immunodeficiency and lymphoma at the California Regional Primate Research Center (L. J. Lowenstine, N. W. Lerche, P. A. Marx, M. B. Gardner, and N. C. Pedersen, p. 174-176, in M. Girard and L. Valette, ed., Retroviruses of Human AIDS and Related Animal Viruses, 1988). Nucleotide sequence analysis of the gag and env regions indicates that SIVstm is an ancient member of the SIV/human immunodeficiency virus type 2 group; it is quite divergent from known SIVs isolated from African sooty mangabeys as well as from Asian macaques. Furthermore, of all SIV strains described to date, SIVstm is the most closely related to human immunodeficiency virus type 2.
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PMID:A highly divergent simian immunodeficiency virus (SIVstm) recovered from stored stump-tailed macaque tissues. 194 58

A highly conserved sequence near the N-terminus of all human (HIV) and simian (SIV) immunodeficiency virus gag polyproteins appears to be a precursor for a viral mimic of the amidated C-terminus of human gonadoliberin. The gag polyproteins are known to be myristylated; processing of the amidation site would yield myristylated 23-residue peptides whose C-terminal sequences mimic gonadoliberin and presumably behave as ligands for the gonadoliberin receptor. This paper describes the discovery of conserved gonadoliberin-precursor-related sequences in HIV and SIV gag polyproteins and in the p-17 core proteins derived from them. Arguments are presented that the conserved precursor structure requires post-translational processing to a peptide amide derivative which is a ligand for the gonadoliberin receptor. A model has been developed for entry of the viral genomic RNA into host cells through the gonadoliberin receptor and experiments are suggested to confirm or refute the model. This proposed mechanism for entry of HIV genomic RNA into host cells, if it proves to be substantially correct, suggests several new approaches to prevention and treatment of acquired immunodeficiency syndrome (AIDS).
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PMID:A sequence related to the human gonadoliberin precursor near the N-termini of HIV and SIV gag polyproteins. 194 31

Simian immunodeficiency virus from sooty mangabey monkeys (SIVsmm), a lentivirus closely related to SIV from macaques and the human immunodeficiency virus type 2 (HIV-2), is pathogenic for various species of macaques but is nonpathogenic for mangabeys. Comparison of in vivo and in vitro responses of macaques and mangabeys or their lymphocytes, respectively, to SIVsmm infection indicated that lack of disease in mangabeys apparently was not due to effective control of virus expression by the immune system because SIVsmm-infected, asymptomatic mangabeys have high viral loads. Failure of mangabeys to develop disease may be related to the fact that the prototype SIVsmm (SMM-9) replicated in, but was not cytopathic for, mangabey CD4+ cells. In contrast, replication of SMM-9 in peripheral blood mononuclear cells from pigtailed macaques resulted in specific loss of CD4+ cells and induction of an AIDS-like disease. A variant of SMM-9, designated SMM-PBj14, was identified, however, that was extremely cytopathic for mangabey CD4+ cells and also induced acute lethal disease in both macaques and mangabeys. Acute disease was associated with extensive lymphoid hyperplasia, which was correlated in vitro with induction of proliferation of PBMC in SMM-PBj14-infected cultures. Infectious molecular clones of SMM-PBj14 exhibited the same in vitro and in vivo properties as SMM-PBj14. Future analysis of chimeric viruses may lead to the identification of specific regions of the viral genome that influence the various in vivo and in vitro properties of these SIVsmm isolates.
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PMID:SIVsmm infection of macaque and mangabey monkeys: correlation between in vivo and in vitro properties of different isolates. 198 Sep 1

The human immunodeficiency virus type 1 (HIV-1) Rev protein is a positive posttranscriptional regulator of viral structural gene expression and essential for virus replication. Rev mediates its effects through interaction with an RNA target sequence, the Rev responsive element (RRE), present within the env mRNA. Previous studies have shown that the basic stretch of amino acids are required for Rev's ability to bind RNA, whereas residues present near the carboxy terminus are essential for full biological activity. Deletion mutagenesis was used to define the minimal domain required for RNA binding and function. We found that amino acids 8 through 67 confer full binding activity, whereas full biological activity requires the presence of residues 8 through 83. The minimal RNA binding sequence of HIV-1 Rev also interacts and functions with the HIV-2 and SIV RRE elements, indicating that the same domain is responsible for the biological activity with different, but related viruses. Mutational analysis of the RRE was also carried out in an effort to further define elements crucial for its function. Our findings indicate that interaction with Rev involves a stretch of three G nucleotides present at the base of a stem loop structure previously shown to be critical for Rev binding. These results suggest that the high degree of secondary structure of the RRE RNA may serve as a guide to bring Rev in contact with a primary nucleotide sequence required for stable protein-RNA association.
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PMID:Mutational analysis of the HIV-1 Rev protein and its target sequence, the Rev responsive element. 202 97

The structural variability of the external glycoproteins of primate immunodeficiency viruses, has, so far, been investigated exclusively by sequence comparison of the respective proviral genomes. We have examined the structural relationship amount the external glycoproteins from three specific human immunodeficiency viruses (HIF-1, HIV-2), three specific simian immunodeficiency viruses from macaques (SIVmac) and three specific SIV from African green monkeys (SIVagm) by peptide mapping. Differences among glycoproteins were most pronounced between HIV-1 and SIVmac, as well as HIV-2. Two specific glycoproteins from independent SIVagm isolates were closely related to HIV-1, whereas the glycoprotein from a third SIVagm isolate was more similar to those of SIVmac and HIV-2. Our analysis reflects the classification of primate immunodeficiency viruses into three groups, the HIV-2 and SIVmac viruses, the green monkey isolates and HIV-1.
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PMID:Structural comparison of the external glycoproteins of human and simian immunodeficiency virus. 204 May 88

Plasma from two rhesus macaques (Macaca mulatta) experimentally infected with the simian immunodeficiency virus (SIV; isolate SIVmac251) enhanced SIVmac infection of a human CD4+ lymphoblastoid cell line, MT-2. Prechallenge plasma samples from these animals and serum from SIV-negative macaques did not enhance infection. Compared with controls, infection enhancement was characterized by the rapid appearance of syncytium formation (3 to 4 days sooner), reverse transcriptase release (10-fold increase), and cytopathic effect (60% cell killing). Enhancement of activity was dependent on the presence of diluted, fresh SIV-negative macaque serum as a source of complement. A requirement for complement was shown by the absence of enhancement in heat-inactivated serum and by dose-dependent inhibition of enhancement in the presence of polyclonal antibody to monkey complement component C3. Monoclonal antibody to CD4 (OKT4a) blocked enhancement completely, while monoclonal antibody to the human complement component C3d receptor CR2 (OKB7) reduced enhancement by greater than 50%, indicating a requirement for CD4 and CR2 in mediating this phenomenon. SIV infection-enhancing activity appeared in macaques soon after experimental inoculation (28 days). The titer increased over time and peaked just prior to the death of both macaques from opportunistic infections and lymphoma. In vitro SIV infection enhancement is nearly identical to the in vitro complement-mediated, antibody-dependent enhancing (C'-ADE) activity observed in human immunodeficiency virus-positive human sera (Robinson et al., Lancet i:790-794, 1988; Robinson et al., J. Acq. Immun. Def. Synd. 2:33-42, 1989). These observations validate the macaque-SIV model for studies of C'-ADE.
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PMID:Antibody-dependent enhancement of simian immunodeficiency virus (SIV) infection in vitro by plasma from SIV-infected rhesus macaques. 215 8

Colonies of nonhuman primates at the Bowman Gray School of Medicine (BGSM) were tested for antibodies to two retroviruses associated with immunodeficiency by indirect immunofluorescence (IFA) and western blot. A total of 471 cynomolgus macaques (Macaca fascicularis), 144 rhesus monkeys (M. mulatta) and 67 stumptail monkey M. arctoides) were tested for SRV-1, and 152 African green monkeys (Cercopithecus aethiops) were tested for SIV. Of the macaques tested, 170 (36%) cynomolgus, 5 (3%) rhesus and 8 (12%) stumptails were positive for SRV-1 antibodies by IFA. Of the African green monkeys, 54 (36%) were IFA positive for SIV antibodies. A total of 143 African green monkeys tested by IFA also were tested by western blot. In the African green monkeys, the IFA had a positive predictive value of 98% and a negative predictive value of 96%. Of 176 IFA positive macaque sera tested by western blot, 49 (28%) were positive, 55 (31%) were considered equivocal (only one band, usually to p27 core protein), and 72 (41%) were negative.
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PMID:Serological survey for two simian retroviruses in macaques and African green monkeys. 215 54

While cell-mediated immunity is known to play an important role in controlling viral infections, its role in human and experimental animal models of human AIDS has not been established. To address this issue, four juvenile rhesus macaques were infected with simian immunodeficiency virus SIVMAC. Freshly isolated peripheral blood mononuclear cells from these SIVMAC-infected macaques and four uninfected control macaques were assessed for T-cell proliferative activity to SIV, monthly, for 10 consecutive months. T cells from SIV-infected monkeys failed to proliferate in response to SIV added directly to the culture. However, when SIV was processed by autologous antigen-presenting cells prior to culture with purified T cells, proliferative responses were uniformly demonstrated in SIV-infected monkeys, but not in uninfected controls. Proliferation in response to heat-inactivated SIV was mediated by CD4+ T cells and was shown to be MHC class II-restricted. However, the proliferative response to infectious SIV was mediated by both CD4+ and CD8+ T cells and was MHC class-restricted. As disease progressed, a decline in the T-cell proliferative response was observed.
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PMID:Simian immunodeficiency virus-specific T-cell-mediated proliferative response of infected rhesus macaques. 216 69

The measurement of cell-mediated immunity against the etiologic agent of human AIDS (HIV) in the non-human primate model of AIDS (simian immunodeficiency virus, SIV) has been difficult. In general, culture of peripheral blood mononuclear cells from HIV-1- and SIV-infected humans and monkeys, respectively, with purified inactivated HIV and SIV virus preparations has given inconsistent or negative proliferative responses. However, we describe herein an assay which consists of coculturing monocytes that have been pulsed with inactivated SIVsmm with nylon-wool-purified autologous T cells, leading to antigen-specific T-cell proliferation. The proliferative response, which predominantly occurs in CD4+ T cells, is major histocompatibility complex (MHC) class II-restricted and requires antigen processing. This assay will greatly facilitate the identification of the immunodominant epitopes recognized by T cells in sooty mangabeys, which are naturally infected but remain clinically asymptomatic, and in rhesus macaques, in which experimental infection leads to clinical symptomatology similar to human AIDS, eventually resulting in death.
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PMID:Requirements for simian immunodeficiency virus antigen-specific in vitro proliferation of T cells from infected rhesus macaques and sooty mangabeys. 216 18


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