Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhesus monkeys infected with simian immunodeficiency virus (SIV) develop a syndrome very similar to patients with acquired immune deficiency (AIDS), including liver disease. This prospective study was undertaken to define the pathology, course, and pathogenesis of liver disease in 20 rhesus monkeys (Macaca mulatta) after intravenous inoculation with the standardized isolate SIV/DeltaB670. Tissue samples from liver and gallbladder between 2 and 24 weeks after inoculation were examined histologically and immunohistochemically for SIV gag protein p26, and by in situ hybridization with an SIV riboprobe. Histologically there was infiltration of portal tracts and around hepatic veins and venules by mononuclear inflammatory cells, focal bile duct damage, proliferation of bile ductules, and focal lobular inflammation as early as 2 weeks after infection. The severity and extent of these lesions were graded semiquantitatively and showed that bile duct damage and hepatic venulitis were the most significant changes. Simian immunodeficiency virus gag protein p26 and SIV RNA were detected in scattered mononuclear cells in portal tracts and sinusoids, but not in hepatocytes or bile duct epithelial cells. The data indicate that the liver is involved early during the course of SIV infection, followed by persistent changes until the terminal stage of the disease. Our findings suggest that the liver damage in SIV-infected rhesus monkeys is similar to the changes observed previously in AIDS patients.
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PMID:Liver disease in rhesus monkeys infected with simian immunodeficiency virus. 195 27

Calves inoculated with bovine immunodeficiency-like virus (BIV) produced virus-specific antibodies that could be detected from 2 weeks to 2.5 years postinoculation by using both indirect fluorescent-antibody and Western immunoblot assays. Antibodies were primarily to p26. Virus and BIV-specific antibodies were isolated from calves given BIV-infected blood. Antibodies to BIV proteins were found in sera from naturally infected cattle.
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PMID:Humoral immune response to the bovine immunodeficiency-like virus in experimentally and naturally infected cattle. 219 Nov 53

We have documented rare infection of baboons in their native habitat with simian immunodeficiency virus (SIV). Of 124 sera collected from yellow baboons in central Tanzania, two gave high readings by SIVagm ELISA (greater than 1.0) and moderate by SIVmac ELISA (0.5-1.0). These two sera gave strong reactions to the major SIVagm proteins, including gp130, by western blot analysis; their reactivity to SIVmac protein was considerably weaker. Similar testing of 155 sera from olive baboons of Ethiopia revealed no clearly positive sera. Thus, 2 of 279 baboon sera or 0.7% were positive for antibodies to SIV. The strong reactivity of the two positive yellow baboon sera with SIVagm proteins raises questions about whether these animals may have been infected by green monkeys in their native habitat; baboons occasionally prey upon and eat green monkeys. In addition to these two clearly positive samples, one olive baboon serum and one yellow baboon serum reacted only with major gag protein (p24-p26). Continued study of prevalence and diversity of SIV in primates will be important for understanding the history and evolution of primate lentiviruses and, it is hoped, the origins of viruses that cause AIDS in humans.
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PMID:Prevalence of antibodies to SIV in baboons in their native habitat. 254 34

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

We describe here a one step HPLC technique for purifying the four gag proteins (p26, p15, p11 and p9) and two env glycoproteins (gp90 and gp45) from purified equine infectious anemia virus (EIAV), a member of the lentivirus subfamily of retroviruses. The purification procedure employs a reverse-phase phenyl Radial-pak cartridge contained in a high pressure radial compression chamber in which a shallow, multistep acetonitrile gradient is applied at ambient temperatures. The purified proteins are recovered at an efficiency of 60-70%. Moreover, the isolated components retain their antigenicity and are suitable for a variety of biochemical analyses including protein sequencing. The purification of EIAV gp90 and gp45 represents the first successful isolation of a lentivirus glycoprotein from purified virus preparations. The availability of these separated proteins permitted direct protein sequencing which confirmed the previously reported env gene sequence and provides important antigens for the development of diagnostic immunoassays and subunit vaccines. The procedures described appear applicable to other lentiviruses, including human immunodeficiency virus (HIV), and perhaps to hydrophobic membrane proteins in general.
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PMID:Lentivirus antigen purification and characterization: isolation of equine infectious anemia virus gag and env proteins in one step by reverse phase HPLC and application to human immunodeficiency virus glycoproteins. 283 62

Electroejaculates from experimentally infected domestic cats were evaluated for the presence of feline immunodeficiency virus (FIV). Virus was isolated from cell-free seminal plasma and seminal cells by cocultivation with a feline interleukin-2-dependent CD4+ T-cell line, in which productive infection was demonstrated by syncytium formation and FIV gag p26 antigen secretion. In addition, an 868-bp segment of the FIV gag provirus gene was identified in cocultured cells by PCR and Southern analysis. A 582-bp fragment of the FIV gag provirus genome was detected by nested PCR and Southern analysis in nonfractionated seminal cells and in sperm purified by a swim-up procedure. This is the first report describing the detection of replication-competent FIV in cell-free and cell-associated forms in domestic cat semen.
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PMID:Detection of feline immunodeficiency virus in semen from seropositive domestic cats (Felis catus). 747 64

U-75875 inhibits human immunodeficiency virus types 1 and 2 and simian immunodeficiency virus (SIV) proteases and blocks Gag-Pol protein processing and viral maturation and replication in vitro. Rhesus monkeys were treated with vehicle alone or with formulated U-75875 at doses of 7 or 20 mg/kg of body weight per day for 26 days by continuous intravenous infusion beginning 6 h prior to intravenous inoculation with 10 monkey 50% infectious doses of SIV Delta B670, and the monkeys were monitored until death. The effects of treatment on the level of SIV p26 antigenemia, the infectious virus titer in serum, and the level of proviral DNA in blood mononuclear cells evaluated by PCR were assessed. SIV infection of the controls resulted in an initial viral antigenemia that began 5 to 10 days postinoculation (p.i.), reached peak values on days 10 to 14 p.i., and lasted for more than 15 days. Proviral DNA was detectable in peripheral blood mononuclear cells by 7 to 11 days p.i., reached the mean peak level by 11 days p.i., and remained at high levels through day 24 p.i. Infectious virus was detected in serum from all of the infected controls by 24 days p.i. Treatment with U-75875 for 26 days resulted in a dose-related delay in the day of the peak level of antigenemia (P = 0.034). The level of proviral DNA in peripheral blood mononuclear cells at 11 days p.i. was significantly decreased in a dose-related fashion in the treated monkeys ( P </- 0.048), with a delay in the attainment of the peak level of proviral DNA in the treated groups. The titer of infectious virus in the serum of the group treated with 20 mg/kg/day was significantly decreased on day 24 p.i. compared with that in the serum of controls ( P = 0.046). Treatment with formulated U-75875 was well tolerated in rhesus monkeys and resulted in an inhibitory effect of SIV in vivo.
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PMID:Effects of U-75875, a peptidomimetic inhibitor of retroviral proteases, on simian immunodeficiency virus infection in rhesus monkeys. 752 27

We generated monoclonal antibodies (MAB) against feline immunodeficiency virus (FIV) and characterized these MAB by single competition enzyme immunoassays (EIA), immunoblot analysis, and radioimmunoprecipitation. Four MAB identified 3 distinct epitopes of the FIV p24/26 gag major core protein. One MAB recognized the p16/17 gag protein; none recognized envelope proteins. We developed an FIV p26 antigen capture EIA that proved more sensitive (0.5 ng of p26/ml), less expensive, and less time-consuming than reverse transcriptase assay. The same MAB were used to develop an antibody EIA specific for FIV p26. The MAB and capture assays reported should prove useful in FIV diagnosis and research.
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PMID:Development of monoclonal antibodies and capture immunoassays for feline immunodeficiency virus. 754 55

An Escherichia coli recombinant fusion protein containing the major core protein of bovine immunodeficiency-like virus (BIV) was used to immunize mice for generation of monoclonal antibodies to BIV p26. Eight hybridomas specific for BIV p26 were identified and two antibodies, designated 104 and 142, were further characterized. Both 104 and 142 antibodies were isotyped as IgG1; they reacted specifically with both BIV p26 and the recombinant fusion protein in Western immunoblot analyses. However, the epitope specificity of the antibodies was different. Immunoperoxidase assays were used to determine if antibodies 104 and/or 142 could detect BIV replication in cell culture. Both antibodies were found to react with BIV-induced syncytia and individual BIV-infected cells. The antibodies were also used successfully in a focal immunoassay for quantitation of BIV-infected cells. These antibodies will provide valuable reagents for detection and quantitation of BIV replication in studies of viral pathogenesis and immunity.
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PMID:In vitro detection of bovine immunodeficiency-like virus using monoclonal antibodies generated to a recombinant gag fusion protein. 769 43

To assess the potential therapeutic effects of zidovudine, rhesus macaques were inoculated with simian immunodeficiency virus (SIV) strain SMM/B670 at birth and infused either continuously or intermittently with zidovudine for 6-7 months. Zidovudine did not prevent infection but did significantly increase survival time, which was associated with lower serum p26 viral core antigen levels, a lower virus burden in the cerebrospinal fluid (CSF), and lower CSF quinolinic acid levels than in untreated monkeys. Two of 5 infected, untreated monkeys developed motor impairment within 6 months following infection, whereas motor impairments did not occur in infected, zidovudine-treated monkeys until after the drug was discontinued. Zidovudine treatment was well tolerated by rhesus infants with minimal, transient side effects. These results demonstrate that zidovudine treatment significantly decreases virus load within the central nervous system (CNS) and delays the onset of CNS dysfunction and immune disease in rhesus monkeys perinatally infected with SIV.
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PMID:Zidovudine treatment prolongs survival and decreases virus load in the central nervous system of rhesus macaques infected perinatally with simian immunodeficiency virus. 779 47


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