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Query: UNIPROT:Q96DT5 (SIV)
 2,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The CD4 antigen has been subverted as a receptor by the human and simian immunodeficiency viruses (HIV-1, HIV-2 and SIV). Several groups have reported that recombinant, soluble forms of the CD4 molecule (sCD4) block the infection of T lymphocytes by HIV-1, as CD4 binds the HIV envelope glycoprotein, gp120, with high affinity. We now report that sCD4 blocks diverse strains of HIV-1, HIV-2 and SIV, but is less effective for HIV-2. The blocking effect is apparent even after adsorption of virions to CD4 cells. Soluble CD4 prevents HIV infection of T-lymphocytic and myelomonocytic cell lines, but neither sCD4 nor anti-CD4 antibodies inhibit infection of glioma and rhabdomyosarcoma cell lines.
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PMID:Soluble CD4 blocks the infectivity of diverse strains of HIV and SIV for T cells and monocytes but not for brain and muscle cells. 253 42

The world now has a pandemic of infection by the human immunodeficiency virus type I (HIV-1). More recently, a focus of epidemic HIV-2 infection in West Africa has been noted and this too is spreading internationally. HIV-2 closely resembles a simian lentivirus, SIV; SIV isolates have now been made from African (but not Asian) old world monkeys and SIV infection in macaques may provide the best animal model for HIV. All of these viruses share a tropism for the CD4 molecule, which is intimately involved in their pathogenesis. The immune response to these viruses has yet to demonstrate any protective immunity.
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PMID:The biology and epidemiology of HIV infections. 254 Nov 25

Because of the close phylogenetic relationship, nonhuman primates are highly susceptible to human pathogens, including infection of chimpanzees by the human immunodeficiency virus (HIV), the causative agent of AIDS. This, and the existence of a highly related simian virus, SIV, which causes an AIDS-like disease in macaques, emphasizes the continued importance of using nonhuman primates as model systems for identifying and developing prophylaxis and therapy for infectious agents and, in particular, for fighting the pandemic AIDS.
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PMID:Nonhuman primates and the acquired immunodeficiency syndrome: a union of necessity. 254 Dec 46

Five healthy cynomolgus monkeys were inoculated intravenously with simian immunodeficiency virus (SIVsm) propagated in human lymphocytes. All five animals became infected. Virus was recovered from blood mononuclear cells and viral antigen was detected in serum 12 days postinoculation (PI) in all inoculated animals. Virus was also isolated in all five animals tested 74 to 226 days PI. Antibodies to different structural proteins of SIV and HIV-2 were demonstrated by ELISA, Western blot, and radioimmunoprecipitation assay from day 31 PI concomitantly with a reduction of viral proteins in the serum. Reappearance of antigen accompanied by a fall in antibody to gag products (p26) was observed in two monkeys 69 days PI. All SIV-infected monkeys showed a pronounced decrease in CD4+ lymphocytes demonstrable already 12 days PI. They also developed persistent lymphadenopathy. Thus, infection of cynomolgus monkeys with SIVsm mimics events in human immunodeficiency virus infection in humans but the course of evolution of pathogenic events in the monkey is markedly compressed. This experimental model will be useful for evaluation of HIV vaccines and antiviral testing.
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PMID:Experimental infection of cynomolgus monkeys (Macaca fascicularis) with simian immunodeficiency virus (SIVsm). 254 56

A tritium-labeled DNA envelope gene probe was used to detect Simian Immunodeficiency Virus in formalin fixed lymph nodes from rhesus monkeys experimentally inoculated with SIVmac251. Cells containing SIV RNA produced strong hybridization signal and were present in small numbers in biopsy specimens and in much greater numbers in lymph nodes collected at autopsy. SIV-infected cells were morphologically identified as lymphocytes and macrophages.
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PMID:Detection of simian immunodeficiency virus in macaque lymph nodes with a SIVmac envelope probe. 254 58

We have demonstrated that the genetic diversity of simian immunodeficiency virus from African green monkeys (SIVagm) is much greater than that observed previously for individual HIV-1, HIV-2, or SIVmac isolates. Extensive genetic variation among SIVagm isolates and the high prevalence of green monkey infection without disease suggest that the virus has been in the green monkey population for a long time. We have also demonstrated that SIV from a sooty mangabey monkey (isolate SMM-7) is closer to SIVmac and HIV-2 than to HIV-1 and SIVagm. The extensive genetic diversity of SIVagm and the relatedness of SIVsmm to HIV-2 warrant continued examination of SIVagm and SIVsmm isolates from dispersed geographic regions. SIV strains much more closely related to HIV-1, HIV-2, or SIVmac may be found which would be reasonable candidates for recent cross-species transmission.
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PMID:Genetic diversity of simian immunodeficiency virus. 256 37

Since the isolation of an HIV-2-related virus from captive macaques (SIVMAC), the origin of human immunodeficiency viruses, a much debated subject, has been attributed to monkeys. The sequence of SIVAGM, which is derived from a naturally infected African green monkey, shows equal relatedness to HIV-1 and HIV-2, suggesting that the derivation of these viruses from SIVAGM is unlikely. Recent sequence analysis of SIV from a captive sooty mangabey (SIVMAC), however, shows its close relatedness to HIV-2 and SIVMAC, indicating a possible origin of HIV-2 and SIVMAC from SIVSM (refs 4, 7, 9). We report here the sequence of a novel simian lentivirus, SIVMND, isolated from a wild-caught mandrill in Africa. It is distinct from the three other main groups, HIV-1, HIV-2/SIVMAC/SIVSM and SIVAGM, and therefore represents a fourth main group of primate lentiviruses. Phylogenetic analysis indicates that these four main virus groups might have diverged from a common ancestor at about the same time, long before the spread of AIDS in humans.
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PMID:Sequence of a novel simian immunodeficiency virus from a wild-caught African mandrill. 279 81

An important point of regulation in the reproductive growth and latency of the human and simian immunodeficiency viruses (HIV and SIV, respectively) is provided by virally encoded trans-activators (tat), proteins capable of dramatically increasing viral gene expression. The mechanism of this autostimulatory pathway has remained unclear, however, with substantial effects having been reported at the level of either mRNA accumulation, translational efficiency, or both. Our previous findings indicated that trans-activation results primarily from induction of RNA levels but could not distinguish between the roles of transcriptional rate, RNA stabilization, and RNA transport in this event. In addition, the boundaries of tat-responding elements, which would be valuable in elucidating the mode of tat action, are not precisely known. In this study, HIV-1 and HIV-2 long terminal repeat-directed expression was characterized by using an in vitro nuclear transcription assay to clarify this mechanism, and a detailed mutational analysis was undertaken to localize precisely the sequences participating in this process. Two key findings were revealed: an increased transcription rate was the primary event in tat-mediated activation of HIV-1 and HIV-2, and trans-activation was impaired by mutations in two regions, the TATA box and sequences between +19 to +42, a region lacking enhancer activity. These results implicate a discrete 3' regulatory element in the transcriptional activation of the HIVs.
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PMID:A discrete element 3' of human immunodeficiency virus 1 (HIV-1) and HIV-2 mRNA initiation sites mediates transcriptional activation by an HIV trans activator. 284 83

Synthetic peptide segments of the CD4 molecule were tested for their ability to inhibit infection of CD4+ cells by the human immunodeficiency virus (HIV) and to inhibit HIV-induced cell fusion. A peptide mixture composed of CD4(76-94), and synthesis side products, blocked HIV-induced cell fusion at a nominal concentration of 125 micromolar. Upon high-performance liquid chromatography, the antisyncytial activity of the peptide mixture was found not in the fraction containing the peptide CD4(76-94) itself, but in a side fraction containing derivatized peptide products generated in the automated synthesis. Derivatized deletion and substitution peptides in the region CD4(76-94) were used to demonstrate sequence specificity, a requirement for benzyl derivatization, and a core seven-residue fragment required for antisyncytial activity. A partially purified S-benzyl-CD4(83-94) peptide mixture inhibited HIV-induced cell fusion at a nominal concentration of less than or equal to 32 micromolar. Derivatized CD4 peptides blocked cell fusion induced by several HIV isolates and by the simian immunodeficiency virus, SIV, and blocked infection in vitro by four HIV-1 isolates with widely variant envelope gene sequences. Purified CD4(83-94) dibenzylated at cysteine 86 and glutamate 87 possessed antisyncytial activity at 125 micromolar. Derivatization may specifically alter the conformation of CD4 holoreceptor peptide fragments, increasing their antiviral efficacy.
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PMID:Synthetic CD4 peptide derivatives that inhibit HIV infection and cytopathicity. 296 19

Human immunodeficiency virus 1 (HIV-1) is the aetiological agent of AIDS. The virus establishes lytic, latent and non-cytopathic productive infection in cells in culture. The complexity of virus-host cell interaction is reflected in the complex organization of the viral genome. In addition to the genes that encode the virion capsid and envelope proteins and the enzymes required for proviral synthesis and integration common to all retroviruses, HIV-1 is known to encode at least four additional proteins that regulate virus replication, the tat, art, sor and 3' orf proteins, as well as a protein of unknown function from the open reading frame called R. Close examination of the nucleic acid sequences of the genomes of multiple HIV isolates raised the possibility that the virus encodes a previously undetected additional protein. Here we report that HIV-1 encodes a ninth protein and that antibodies to this protein are detected in the sera of people infected with HIV-1. This protein distinguishes HIV-1 isolates from the other human and simian immunodeficiency viruses (HIV-2 and SIV) that do not have the capacity to encode a similar protein.
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PMID:Identification of a protein encoded by the vpu gene of HIV-1. 304 30


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