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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant lymphomas associated with human (HIV) and simian (SIV) immunodeficiency virus infections are reviewed and compared. Recent observation of a high frequency of lymphomas in a series of cynomolgus macaques, highly immunodeficient after infection with SIVsm(smm3) are described. In addition to the increased frequency in human and monkey AIDS, SIV and HIV lymphomas share several important features. Clinically and by histology they present as aggressive high-grade malignant tumors with a predilection for extranodal growth in viscera, skin, central nervous system, testis, and retroorbitally. Most malignant lymphomas are of B-cell origin. AIDS lymphomas in humans are heterogeneous with regard to Epstein-Barr virus (EBV) association. Similarly, most lymphomas in monkeys experimentally infected with SIV tested to date were shown to be associated with an EBV-like simian herpes virus. These observations point to the possibility of using SIV-immunodeficient macaques for study of EBV and other oncogenic and immunosuppressive factors in AIDS-associated lymphomagenesis.
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PMID:Malignant lymphoma associated with human AIDS and with SIV-induced immunodeficiency in macaques. 157 Nov 94

Replication competent chimeric viruses that express the gag and pol proteins of SIVmac and the env proteins of HIV-1 were made. One such chimeric virus, SHIV-4, that expresses the vif, vpx, vpr, and nef regulatory genes of SIV and the tat and rev regulatory genes of HIV-1 replicated efficiently in cynomolgus monkeys. This model system can be used to evaluate the efficacy of anti-HIV-1 vaccines directed at the envelope glycoproteins, anti-HIV-1 envelope glycoprotein antiserum or monoclonal antibodies, and anti-HIV-1 drugs designed to inhibit the tat, rev, or env functions.
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PMID:Infection of cynomolgus monkeys with a chimeric HIV-1/SIVmac virus that expresses the HIV-1 envelope glycoproteins. 161 62

The transmission of human immunodeficiency virus (HIV-1) and other enveloped virus by blood transfusion is a major concern. Photosensitive dyes such as hematoporphyrin derivative (HPD), dihematoporphyrin ether (DHE), benzoporphyrin derivatives (BPD), extended ring porphyrins, sapphyrins and texaphyrins, and various cyanines were used with viral cultures to test the feasibility of using those light-excitable dyes to kill virus. A photodynamic flow cell was used to irradiate viral suspensions or viral infected cells in culture media or in whole blood. Herpes virus (HSV-1) was used to screen compounds. Effective compounds were subsequently tested for their ability to kill HIV-1, CMV, and SIV in culture medium and in blood and proved to effectively kill free virus and infected cells at significant viremias. Irradiation was achieved with a filtered xenon light source and/or tunable dye laser. Concentrations of dyes at 10 times viral kill dose were irradiated in blood which was tested for damage to erythrocytes (RBC), platelets, and blood proteins. No damage to RBC, complement factors, and immunoglobulins was evident immediately after photodynamic treatment. Platelet condition is minimally modified with time. Photodynamic treatment of blood appears to be a feasible means of eradicating virus and some protozoans from blood.
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PMID:Inactivation of viruses with photoactive compounds. 161 95

A simple, reliable ELISA for the quantitative detection of the envelope glycoproteins of both HIV and SIV is described. It incorporates the snowdrop lectin GNA to capture the glycoprotein antigens and combines the high selectivity of GNA binding with its broad reactivity with the glycoproteins of HIV-1, HIV-2 and SIV.
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PMID:An ELISA utilizing immobilised snowdrop lectin GNA for the detection of envelope glycoproteins of HIV and SIV. 162 22

Previous studies showed that apoA1, the major protein component of HDL (High Density Lipoprotein), inhibited HIV infectivity and virus-induced syncytia formation. The mechanism of inhibition is unknown. We bring here evidence that the amphipathic helices of apoA1 interact with the N-terminal peptides of SIV gp32 and HIV gp41. These peptides have been shown to be associated with the initial steps of the fusion between the host cell and the virus. Binding of apoA1 to these peptides prevents the insertion of the fusogenic domains into the cell membrane and inhibits the fusion and the entry of the virus into the host cell.
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PMID:Apolipoprotein A-1 interacts with the N-terminal fusogenic domains of SIV (simian immunodeficiency virus) GP32 and HIV (human immunodeficiency virus) GP41: implications in viral entry. 163 97

The promoter activity of long terminal repeats (LTRs) of four strains of the simian immunodeficiency virus isolated from African green monkeys (SIVAGM) was compared with those of various LTRs derived from the other representative primate lentiviruses: human immunodeficiency virus type 1 (HIV-1), type 2 (HIV-2), SIV from a rhesus monkey (SIVMAC), and SIV from a mandrill (SIVMND). The expression of the LTRs was evaluated by monitoring chloramphenicol acetyltransferase production after transfection of reporter plasmid clones. In the absence of viral tat, all SIVAGM LTRs acted as much more efficient promoters than any of the other LTRs. When tat gene products were supplied in trans, LTRs of SIVAGM and SIVMND were activated inefficiently relative to high responder LTRs of HIV-2 and SIVMAC. The LTR of HIV-1 was highly activated by HIV-1 tat, but not so much by HIV-2, SIVAGM, and SIVMND tat.
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PMID:Functional analysis of long terminal repeats derived from four strains of simian immunodeficiency virus SIVAGM in relation to other primate lentiviruses. 165 99

Visna virus, a lentivirus of sheep, causes fusion of susceptible cells. Fusion has previously been shown to be mediated by the viral envelope glycoprotein. The transmembrane protein of visna virus contains a hydrophobic region at its amino terminus. This region is similar to the fusion epitopes of the orthomyxoviruses and paramyxoviruses. This region is located in a position similar to that of the fusion epitopes in the transmembrane proteins of HIV-1 and SIV. To determine the role of this hydrophobic region in visna virus-induced cell fusion, a peptide of 24 amino acids corresponding to this region was synthesized. The peptide alone induces fusion of goat cells. Antibodies to this peptide inhibit both viral-induced cell fusion and peptide fusion in goat cells. Further, the direct fusion of cells by this peptide is a unique observation and may be useful for studying the fusion epitopes of other lentiviruses. Thus, this hydrophobic region appears to be one epitope responsible for visna virus-induced cell fusion.
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PMID:Identification of the fusion domain in the visna virus transmembrane protein. 165 2

Although oncoviruses and lentiviruses replicate by similar mechanisms, they differ fundamentally in the usual fate of the infected host cell during productive natural infections. Oncoviruses typically establish persistent nonlytic infections in natural host cells, while lentivirus infections characteristically result in a variety of cytopathic effects ultimately leading to death of the target cell. Described here is a unique structural motif consisting of a strongly amphipathic and arginine-rich helical peptide segment in the carboxyl end of lentivirus TM proteins that is structurally similar to the family of cytolytic peptides produced as defensive agents by certain insects and amphibians. Also demonstrated is the lytic nature of synthetic peptides constructed from the transmembrane (TM) protein of human and simian immunodeficiency viruses (HIV and SIV). Thus, it appears that the cytopathic properties of lentiviruses may be in part attributed to the presence of lytic peptides within the TM protein, designated lentivirus lytic peptide (LLP) and that variations in this segment could account for some of the differences observed in the cytopathicity among variants of a particular lentivirus.
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PMID:A structural correlation between lentivirus transmembrane proteins and natural cytolytic peptides. 165 72

To develop a nonhuman primate model for maternal-fetal transmission of HIV infection, we have inoculated pregnant Macaca nemestrina with uncloned SIVMne. Three animals inoculated during the third trimester delivered healthy infants. One of the three infants, a male born 31 days after the mother was inoculated with SIV, became virus-positive but failed to produce SIV-specific antibody and died with overt simian immunodeficiency and disseminated adenovirus (SV20) infection at age six and one-half months. SIV and adenovirus antigen could be demonstrated by immunohistochemical methods in multiple organ systems.
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PMID:Maternal-fetal transmission of SIV in macaques: disseminated adenovirus infection in an offspring with congenital SIV infection. 165 26

RNA pseudoknot structural motifs could have implications for a wide range of biological processes of RNAs. In this study, the potential RNA pseudoknots just downstream from the known and suspected retroviral frame-shift sites were predicted in the Rous sarcoma virus, primate immunodeficiency viruses (HIV-1, HIV-2, and SIV), equine infectious anemia virus, visna virus, bovine leukemia virus, human T-cell leukemia virus (types I and II), mouse mammary tumor virus, Mason-Pfizer monkey virus, and simian SRV-1 type-D retrovirus. Also, the putative RNA pseudoknots were detected in the gag-pol overlaps of two retrotransposons of Drosophila, 17.6 and gypsy, and the mouse intracisternal A particle. For each sequence, the thermodynamic stability and statistical significance of the secondary structure involved in the predicted tertiary structure were assessed and compared. Our results show that the stem-loop structures in the pseudoknots are both thermodynamically highly stable and statistically significant relative to other such configurations that potentially occur in the gag-pol or gag-pro and pro-pol junction domains of these viruses (300 nucleotides upstream and downstream from the possible frameshift sites are included). Moreover, the structural features of the predicted pseudoknots following the frameshift site of pro-pol overlaps of the HTLV-1 and HTLV-2 retroviruses are structurally well conserved. The occurrence of eight compensatory base changes in the tertiary interaction of the two related sequences allow the conservation of their tertiary structures in spite of the sequence divergence. The results support the possible control mechanism for frameshifting proposed by Brierley et al. and Jacks et al.
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PMID:RNA pseudoknots downstream of the frameshift sites of retroviruses. 166 82


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