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 a study population representing different CDC stages of HIV infection, 58% exhibited IgA hypergammaglobulinemia resulting from proportional increases in both the IgA1 and the IgA2 subclasses. These increases were detected early in infection, did not correlate with CD4 count, and remained elevated throughout disease progression. Absolute concentrations of polymeric IgA present within each subclass were unchanged, indicating that increased production of monomeric IgA1 and IgA2 were responsible for elevations of total IgA. These elevations were not completely attributable to a specific antibody response to viral infection, since Western blot analysis of purified IgA samples indicated that HIV-reactive IgA antibodies could be demonstrated only within the IgA1 subclass. Dominating IgA1 anti-HIV responses were also observed in two secretory IgA samples isolated from colostrum of healthy HIV seropositive mothers, suggesting that a similar isotype restriction exists in the mucosal IgA compartment. The binding of IgA1 to HIV proteins contrasted markedly to that observed with identical concentrations of IgG purified from the sera of the same patients. While IgG reacted more intensely and broadly with all HIV proteins, IgA1 antibodies were directed predominantly against envelope glycoproteins. In many patients, a total lack of IgA1 reactivity to gag and pol proteins was accompanied by intact IgG responses to these same antigens. Though all IgA samples examined reacted with HIV, fewer responses to gp160, gp120, and p24 were observed in samples from AIDS and AIDS-related complex (ARC) patients, suggesting a declining titer of IgA antibodies against these antigens may be associated with disease progression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum IgA subclasses and molecular forms in HIV infection: selective increases in monomer and apparent restriction of the antibody response to IgA1 antibodies mainly directed at env glycoproteins. 145 91

We have shown previously that HIV-1 matrix protein p17 is transported to the nucleus of Jurkat-tat and H9 cells soon after infection. As shown in this combination, gag polyprotein p55 synthesized 48 h after cell infection is cleaved in cytosol rapidly after its synthesis, and nascent p17 enters the nuclei and gradually accumulates there. Uncleaved p55 molecules and intermediate precursors are rapidly transported to the membranes and are also found in nuclei. Mature gag proteins are seen in membranes only after prolonged period of labelling or chase (4 or more hours later). To determine whether the nascent p17 is associated with viral genomic RNA in the nuclei, the cells were fractionated, the viral complexes were immunoprecipitated by monoclonal antibodies (MAbs) against gag proteins, and RNA was extracted and analyzed by slot and blot hybridization. MAb against p17 precipitated all the viral RNA from the nuclei including full-size genomic RNA and essential parts from membranes while MAb against p24 did not precipitate any viral RNA from the nuclei. These data suggest that matrix protein is linked to genomic RNA in the nuclei and raise the possibility that p17 may transfer viral nucleocapsids from the nuclei to plasma membranes, the site of virus assembly.
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PMID:HIV-1 matrix protein p17 resides in cell nuclei in association with genomic RNA. 145 92

An in vitro model has made it possible to demonstrate HIV transmission from infected lymphocytes to placental trophoblast cells via endocytosis. Upon addition to cultured trophoblast cells (BeWo), chronically HIV-infected lymphocytic cells (MOLT-4) adhered to the epithelial cells via a complex of newly induced microvilli. Though viruses were infrequently seen in the infected lymphocytic cell line, mature virions appeared promptly and profusely in the interstices between the interdigitating microvilli of the two cell types. Virions appeared to bud from the lymphocyte donor cells at the point of cell-to-cell contact and were rapidly taken up by the trophoblast cells via an endocytic mechanism involving coated pits, endosomes, and lysosomes. Electron microscopic observations suggest that HIV may later escape into the trophoblast cytoplasm by fusing with the endosome membrane or by lysing the lysosome membrane. Coincubation for 1 h was sufficient to establish HIV infection in the trophoblast cell line. Four weeks after thoroughly washing out the donor lymphocytic cells, HIV RNA was demonstrated in clusters of BeWo cells by in situ hybridization, and p24 antigen was localized with immunocytochemistry. Soluble CD4 did not block infection as measured by p24 ELISA. The HIV infection was productive and chronic as demonstrated by cocultivating the BeWo cells with indicator lymphocytes 4 weeks after the initial infection. This study, demonstrating a mechanism of HIV transmission, expands upon previous observations that trophoblast cell lines lacking the CD4 viral receptor can nevertheless be infected by HIV and can support productive infection.
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PMID:HIV-1 infection of the trophoblast cell line BeWo: a study of virus uptake. 145 13

The analysis of human immunodeficiency virus type 1 (HIV-1) RNA sequences in CEM and Jurkat lymphoid cells infected with the virus has been performed at the subcellular level. Using a biotinylated DNA probe specific for HIV-1, virus RNA sequences were detected on Lowicryl thin sections after immunogold cytochemistry. The labelling observed on the cytoplasm was localized near the plasma membrane connected with extracellular cluster of virions. On free immature and nascent form of the virus the detection of HIV-1 RNA was associated with the peripheral electron-dense structure, whereas on mature form the labelling was concentrated on the central nucleoid known to be the site of the HIV-1 genomic RNA. The identification of virus RNA was also performed simultaneously with the detection of HIV-1 core protein p24 or p17 using a double immunogold labelling. Whereas the HIV-1 RNA showed again a cytoplasmic and virions localization, the structural protein was only observed on viral formations. The cytoplasmic localization of virus RNA, at the time of virus production, suggests that they are of genomic origin destined to be packaged in virions once the assembly of virus structural proteins has taken place in the plasma membrane at the viral budding site. The present molecular investigation conducted at the subcellular level provides insight into the cell periphery distribution of HIV-1 RNA observed at the light microscope as corresponding to the detection of HIV-1 infected lymphoid cells actually releasing virions.
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PMID:Ultrastructural localization of HIV-1 RNA and core proteins. Simultaneous visualization using double immunogold labelling after in situ hybridization and immunocytochemistry. 145 33

HIV-1 p24 antigen was detected in 554 sera (509 from HIV-1 seropositive individuals and 45 sera from seronegative controls) using a conventional method with acid pretreatment of the sample in order to separate the p24 antigen/anti-p24 antibody immune complexes. In asymptomatic individuals there was a substantial increase in antigen detection (48.2% vs 8.4%). Similar results were also observed in ARC (59.1% vs 12.2%) and AIDS patients (85.7% vs 37.1%). It can be concluded that the acid treatment improves the sensitivity of conventional techniques to detect HIV-1 p24 antigen.
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PMID:Improved detection of HIV p24 antigen in serum after acid pretreatment. 146 28

The incidence of various patterns of antibodies against HIV 1 proteins was tested by Western blot in EIA--positive serum samples from intravenous drug abusers. The presence of anti-p24, anti-gp160 and anti-gp120 antibodies was the most typical pattern suggestive for early humoral response. In most instances of indeterminate results subsequent WB tests performed during 4 to 6 week period showed whole spectrum of anti-HIV 1 antibodies.
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PMID:[Diagnostic value of antibodies against HIV-1 proteins in seropositive drug addicts tested by the western blotting method]. 147 86

The pharmacokinetics of oral administration of R 82913, or tetrahydroimidazol [4,5,1-jk]-benzodiazepin-2(1H)-one or -thione (TIBO), was compared with those of intravenous administration in five AIDS patients. TIBO was administered as a single daily 1-h infusion of 100 mg for 29 days and orally as a single daily dose for 14 days with three consecutive regimens of 100, 200, and 100 mg with probenecid (1 g) daily. Each cycle was followed by a wash-out period. Oral bioavailability of TIBO appears to be low and is not improved by the adjunction of probenecid. Trough levels obtained with oral administration systematically remained far below the 90% inhibitory concentration of TIBO against human immunodeficiency virus type 1 (HIV-1). Tolerance of TIBO was excellent. No clinical efficacy could be demonstrated. p24 antigenemia decreased significantly in one patient under intravenous therapy. TIBO derivatives are promising anti-HIV-1 agents in vitro, but improvement of oral bioavailability is needed before implementation of long-term efficacy and tolerability studies. Moreover, rapid emergence of resistance, which has been recently documented, constitutes a major problem with most nonnucleoside reverse transcriptase inhibitors.
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PMID:Pharmacokinetics of R 82913 in AIDS patients: a phase I dose-finding study of oral administration compared with intravenous infusion. 148 34

We have used the ELISPOT assay in combination with ELISA procedures for rapid evaluation of properties of three different murine hybridoma cell lines, 104-I, -B and -G, secreting IgG1 kappa monoclonal antibodies against a 104-mer synthetic peptide from the C-terminal part of HIV-1 p24. By conventional ELISA we obtained data suggesting that the three monoclonal antibodies had different affinities. By cell-ELISA we found that the IgG1 kappa secretion rate varied between cells (4,000 to 14,000 antibody molecules/cell/min), and ELISPOT showed that only 4-5% of 104-I cells gave antigen-specific spots, indicating a cell population with diverse properties. We recommend that the ELISPOT and cell-ELISA techniques should be used routinely to supplement conventional ELISA procedures for rapid evaluation of hybridoma properties.
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PMID:Rapid quality evaluation of hybridomas using ELISPOT and cell-ELISA techniques. 148 2

A group of 41 peptides, each 24 amino acids long and overlapping with each other by 12 residues spanning the total gag open reading frame (orf) of HIV-1 (HTLV-IIIBH 10 isolate) were synthesized using Fmoc chemistry. The purified compounds were used in ELISA assays and tested for antibody reactivities in sera of human HIV-1-infected and noninfected individuals. Sera of HIV- humans showed reactivity against four defined regions, two in p17, one in p24, and one in p15. The values of these reactivities were elevated especially in serum samples of HIV- individuals showing cross-reaction with gag proteins on Western blot. Amino acid sequence comparison of HIV-1 gag proteins with those of human endogenous retroviruses (ERV K10, ERV 3) revealed significant similarities predominantly in the domains showing elevated antibody cross-reactions. The majority of sera from HIV-1+ individuals showed strong reactivities to the cross-reactive regions and to various other peptide sequences, a sequential epitope recognized by all HIV-1+ sera could, however, not be identified. The results suggest that human individuals may have immune reactions to endogenous retroviral protein sequences, which are enhanced by infections with HIV-1. Specific antibodies to HIV-1 gag proteins are probably mainly directed to tertiary structure defined epitopes formed by particle formation of the p24 monomers to the nucleocapsid.
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PMID:Reactivities of HIV-1 gag-derived peptides with antibodies of HIV-1-infected and uninfected humans. 148 79

Rectal mucosal biopsy specimens from 75 human immunodeficiency virus (HIV)-seropositive and 16 HIV-seronegative subjects were examined. The histopathologic changes were correlated with immunoperoxidase staining for UCHL-1 and HIV core protein p24, quantitative p24 enzyme-linked immunosorbent assay (ELISA) assay in homogenized rectal tissue and serum, and a modified Walter Reed clinical stage. Four phases were seen in the HIV-infected subjects: (1) early phase, in Walter Reed stage 1-2 subjects, with nearly normal histology and low p24; (2) inflammatory phase, typically in Walter Reed stage 3-4 subjects, with a superficial lamina propria infiltrate of lymphocytes, plasma cells, and eosinophils with degranulation, abundant UCHL-1 staining, and maximal p24 by both immunoperoxidase staining and ELISA; (3) transitional phase, in many Walter Reed 5 and some Walter Reed 6 subjects, with normal lymphocyte population density but with subtle inflammatory changes; and (4) lymphoid depletion phase, mainly in Walter Reed stage 6 subjects, with decreased lymphocytes but often with endothelial cell activation and apoptosis. These phases presumably result from effective HIV suppression by a relatively intact immune system, followed by maximal HIV infection and lymphocyte activation, then progressive lymphocyte depletion. The inflammation correlated with the presence and amount of HIV in rectal tissue determined by immunohistochemistry and ELISA and was maximal before overt immunodeficiency developed. Intestinal mucosa could be a preferred site of HIV proliferation and T-cell destruction.
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PMID:Rectal mucosal pathology varies with human immunodeficiency virus antigen content and disease stage. 149 43


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