Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In HuT 78 cells chronically infected with SIV, super-infection with rhesus cytomegalovirus (rhCMV) stimulated an increase in SIV replication. Utilizing transient expression assays with the SIV long terminal repeat (LTR) driving expression of the chloramphenicol acetyltransferase (CAT) reporter gene, the increase in SIV replication, by coinfection with CMV, was due to transactivation of the SIV LTR by the immediate early gene products (IE) of rhesus CMV. Similarly, IE of human CMV stimulated expression from both the SIV and HIV LTRs.
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PMID:Molecular interactions of cytomegalovirus and the human and simian immunodeficiency viruses. 217 42

The SIV macaque model is an excellent surrogate for SIV infection of humans. Genital mucosal transmission of SIV presents the opportunity for testing the effectiveness of spermicides, pharmacologic agents and vaccines in preventing the heterosexual transmission of HIV. Because the incubation period is usually shorter and the disease tempo more rapid than seen with HIV infection, the endpoint for therapeutic, prophylaxis and vaccine trials can be reached sooner in the monkey model. Initial vaccine experiments using inactivated whole SIV mac did not protect rhesus macaques against IV or genital mucosal challenge with a moderately high dose of homologous live virus but did appear to delay disease in the IV challenge group. Similarly, a modified live SIVmac immunogen also failed to protect rhesus monkeys against IV challenge with live virus but did delay disease. It appears, therefore, that a strong immediate immune response to SIVmac, whether naturally or artificially induced can reduce the level of viremia and delay the onset of clinical SAIDS. We believe that these inactivated whole virus and modified live virus approaches are worth pursuing further and they may guide us towards an eventual effective vaccine for AIDS.
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PMID:SIV infection of macaques: a model for AIDS vaccine development. 217 24

The functional exchangeability of the rev gene was assessed in transient transfection experiments by using in vitro-constructed rev and gag mutants of the following three primate lentiviruses: human immunodeficiency virus type 1 (HIV-1), HIV-2, and simian immunodeficiency virus from the African green monkey (SIV AGM). Cotransfection into SW480 cells of the rev and gag mutants derived from the DNA of each infectious virus resulted in the generation of progeny particles as determined by reverse transcriptase assay. rev gene mutants of HIV-2 and SIV AGM were also complemented by all gag mutants derived from the three viruses. In contrast, no evidence of complementation was obtained following cotransfection of the HIV-1 rev mutant and the gag mutant of HIV-2 or SIV AGM.
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PMID:Complementation of the rev gene mutation among human and simian lentiviruses. 218 9

In designing antiviral drugs and therapeutic schemes some basic considerations should be taken into account: 1. RNA viruses and especially HIV (Human Immunodeficiency Virus) respond to environmental changes with evading mutations, hence, the high degree of variability of these viruses. All drugs interfering with viral functions will presumably give rise to resistant variants. 2. Approaches using cytotoxic peptides may induce adverse immune responses. Vaccines may elicit neutralizing antibodies, cellular cytotoxic responses, or both. The limitations of subunit vaccines or oligopeptides in eliciting cell mediated cytotoxicity in all vaccinees are outlined. Recent developments and the suitability of the SIV mac/rhesus monkey model are reviewed. The importance of adjuvants is indicated.
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PMID:Strategies in therapy and immunoprophylaxis of human immunodeficiency virus infection. 218 39

Single-cell clones of HIV-1 (FRE-3) or SIV/Mne infected HuT 78 cells were obtained by plating dilutions of virally infected HuT 78 cells on a monolayer of sheep choroid plexus cells in 96-well microtiter plates. Several of these clones produce HIV-1 virus mutants that accumulate the gag precursor polyprotein and lack a functional protease. These protease-deficient viruses are non-infectious and consist of aberrant "immature" virus particles as determined by electron microscopy. Several SIV mutants are also described that produce large amounts of either the envelope glycoprotein gp120 or the nucleic acid binding gag protein. These mutants are useful for the purification of these retroviral proteins, in developing assays of protease inhibitors, and in preparing SIV envelope protein vaccines.
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PMID:Characterization of clones of HIV-1 infected HuT 78 cells defective in gag gene processing and of SIV clones producing large amounts of envelope glycoprotein. 223 88

The complete nucleotide sequence of an HIV-2 isolate derived from a German AIDS patient with predominantly neurological symptoms is reported. The HIV-2BEN sequence is highly divergent from those of previously described HIV-2 and SIV strains. Evolutionary tree analysis of eight HIV-2 sequences reveals the existence of three HIV-2 groups. HIV-2BEN belongs to a group with two isolates from Ghana and The Gambia. Based on a comparison of HIV-2BEN with six HIV-2 isolates, SIVsmm and SIVmac, the variability of the structural env and gag proteins is similar within the HIV-2/SIVsmm/mac and HIV-1 groups. In contrast, the regulatory HIV-1 proteins are more highly conserved than those from HIV-2 strains. Multiple sequence alignments reveal that some domains of the envelope and regulatory proteins are well conserved among HIV-1, HIV-2/SIVsmm/mac, SIVagm and SIVmnd. The identification of conserved domains within the external glycoprotein could help to develop broadly active vaccines.
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PMID:Genomic divergence of an HIV-2 from a German AIDS patient probably infected in Mali. 225 59

An 80-kilodalton glycoprotein (gp80) was produced in human immunodeficiency virus type 2 (HIV-2)-infected cells along with three envelope glycoproteins that we have recently reported: the extracellular glycoprotein (gp125), the envelope glycoprotein precursor (gp140), and the transient dimeric form of the precursor (gp300). gp125 and gp80 were detectable after the synthesis of gp140 and the formation of gp300. Using a specific monoclonal antibody, we showed here that gp80 is a dimeric form of the transmembrane glycoprotein gp36 of HIV-2. Dimerization of the envelope glycoprotein precursor and dimeric forms of the transmembrane glycoproteins were also observed in cells infected with simian immunodeficiency virus (SIV-mac), a virus closely related to HIV-2. Under routine conditions of our experiments (i.e., extraction by 1% Triton X-100 before polyacrylamide gel electrophoresis in sodium dodecyl sulfate [SDS]), monomeric forms of the transmembrane glycoprotein of HIV-2 and SIV-mac were only seldomly observed. Dimeric forms of the envelope precursors and the transmembrane glycoproteins are probably stabilized by extraction in the nonionic detergent Triton X-100 since such dimeric forms resist dissociation during subsequent electrophoresis in the presence of the ionic detergent SDS. However, the dissociation of these dimeric forms might occur when samples are prepared by extraction directly in 1% SDS or by incubation of the purified dimers at acidic pH. Dimerization of the envelope precursor might be required for its processing to give the mature envelope proteins, whereas the transmembrane dimer might be essential for optimal structure of the virion and thus its infectivity.
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PMID:Transmembrane envelope glycoproteins of human immunodeficiency virus type 2 and simian immunodeficiency virus SIV-mac exist as homodimers. 229 88

Immunoelectron microscopy was applied to study the antigenic make-up of human and simian immunodeficiency viruses (HIV, SIV) grown in cells expressing either MHC class I (Molt-3) or MHC class I and II (H9) antigens. A variety of antibodies directed against the surface glycoprotein gp120 of HIV and against MHC class I and II antigens were employed. Consistent with earlier observations on the loss of HIV envelope components, gp120 was only weakly demonstrable on the mature virion. MHC class I determinants were present regularly in small amounts on HIV and SIV. Class II antigens, e.g. HLA-DR were found in high density on HIV and SIV grown in H9 cells, but were absent, as expected, on virus grown in Molt-3 cells. These cellular surface antigens are constituents of the virion. The presence of MHC class II antigens in virus preparations used for diagnostic purposes might explain some of the false positive results in HIV serology. Possible biological implications of these virus associated cellular antigens for the pathogenicity of HIV are discussed.
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PMID:MHC-antigens: constituents of the envelopes of human and simian immunodeficiency viruses. 245 27

The envelope glycoproteins of HIV, gp120 and gp41, contain epitopes recognized by neutralizing antibodies. Studies of human sera from infected individuals indicate that group-specific neutralization antigens common to most isolates of HIV-1 exist, and that some HIV-2 antisera cross-neutralize HIV-1. Neutralization epitopes for HIV-1 have been identified and mapped, including a group-specific antigen on gp41, and a type-specific antigen on gp120. Neutralization "escape" mutants have been selected in vitro with a neutralizing mab to the type-specific antigenic loop. The CD4 antigen binds HIV-1 gp120 with high affinity and acts as the receptor on human and simian T-lymphocytes and monocytes for all strains of HIV-1, HIV-2, and SIV tested. Following binding to the CD4 receptor, HIV becomes internalized by a pH-independent process. The principle binding domain for gp120 is located in the N-terminal V domain of CD4. Anti-idiotypic sera to CD4 mabs recognizing the same site weakly neutralize HIVs of many strains, and soluble, recombinant forms of CD4 strongly neutralize HIV. Neither anti-CD4 mabs nor sCD4 inhibit the low level of plating of HIV observed on tumour cells in culture of glial (brain) and muscle origin, indicating that CD4 is not essential for infection of these cell types.
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PMID:Human immunodeficiency viruses: neutralization and receptors. 246 1

HIV-1 is predominant in Central and East Africa, while HIV-2 is predominant in West Africa. The HIV-2 virus, originally described as human T-lymphotropic virus type IV, is identical to the simian immunodeficiency virus SIV-mac. Whole-antigen enzyme-linked immunosorbent assay (ELISA) can detect heterotypic antigens in 80% of sera, but separate tests are required for detecting HIV-1 and HIV-2. Site-directed ELISA using amino acids 586-620 of the synthetic transmembranous protein gp41 as antigen has been used for type-specific antibody determination in HIV-1. The homologous site on the 23-amino-acid-long peptide AIEKYLEDQAQLNAWGCAFRQVC representing the transmembranous protein gp32 in the simian immunodeficiency virus SIV-mac is WGCAFR, which can be used in site-directed serology of HIV-2. This approach was tested on sera from 567 Africans in Guinea-Bissau and 49 suspected AIDS patients. None of these sera had HIV-1 antibodies. 93 HIV-1-positive sera from Sweden were used as controls. The HIV-2 peptide ELISA correctly identified 89 of the 90 HIV-2 seropositives out of the sample of 567. The peptide ELISA also correctly identified all of the 93 HIV-1-positive sera as HIV-2-negative. Use of HIV-2-specific ELISA in combination with an HIV-1-specific ELISA can efficiently screen blood for both types of HIV.
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PMID:Site-directed enzyme-linked immunosorbent assay with a synthetic simian immunodeficiency virus SIVmac peptide identifying antibodies against the HIV-2 transmembrane glycoprotein. 246 36


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