Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Seven human immunodeficiency virus gag polypeptides were identified in the purified virus and in infected CD4+ lymphocytes by peptide mapping and limited amino acid sequencing of immune-purified proteins. Two gag polyproteins of 55,000 (p55) and 41,000 (p41) daltons were rapidly labeled and readily processed into the major internal gag proteins that were aligned within the gag open reading frame (ORF) as NH2-p16 (MA)-p24 (CA)-p9 (NC)-p7-COOH. The myristoylated p16 (matrix, MA) protein was processed from the myristoylated p55 gag precursor protein. The immunoreactivity of the p16 (MA) protein with region-specific gag antisera and the conservation of the N-terminal myristyl group of the p55 precursor protein in p16 (MA) confirmed its position as the N-terminal-most protein. The p9 (nucleocapsid, NC) protein was localized to residue 378 of the gag ORF, next to the C terminus of the p24/p25 (core antigen, CA) protein. The p9 protein had a repeating Cys residue containing motif which is found in the nucleic acid-binding Cys residue-containing proteins of retroviruses. The p24 (CA) protein, which was localized to residue 133 of the gag ORF, was apparently derived by C-terminal processing of an intermediate polypeptide, p25. Both the mature p24 (CA) and p16 (MA) proteins were phosphorylated at Ser residue(s). We also identified two forms of gag p41 species, one resulting from the C-terminal processing of p55 and the other originating either from N-terminal processing of p55 or from de novo synthesis.
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PMID:The gag gene products of human immunodeficiency virus type 1: alignment within the gag open reading frame, identification of posttranslational modifications, and evidence for alternative gag precursors. 326 76

An accurate, fast and simple method is presented for synthesis of a gene, or any DNA fragment with a defined sequence. The method is based on the observation that large (approx. 100 bp long) inserts can be cloned into a plasmid using a technique of oligodeoxynucleotide (oligo)-directed double-strand (ds) break repair. The procedure involves transformation of Escherichia coli with a denatured mixture of an insert-carrying oligo and linearized plasmid DNA [Mandecki, Proc. Natl. Acad. Sci. USA 83 (1986) 7177-7181]. The nucleotide (nt) sequences are inserted between two FokI restriction nuclease sites in one of four pUC-derived plasmids. Since FokI makes a staggered ds break at a DNA site 9 and 13 nt away from its recognition site, upon cleavage of the plasmid DNA with FokI, a restriction fragment is liberated that by design contains unique 4-nt-long 5'-protruding ends. The uniqueness of ends permits efficient and directed simultaneous ligation of several restriction fragments to form a gene. The method offers flexibility due to the modular-type assembly and does not require any restriction sites within the constructed gene. The sequence error rate is low: about one error per 4000 bp of DNA cloned. Synthetic DNA for only one DNA strand needs to be provided. The method was applied to the synthesis of a gene fragment encoding the N-terminal 143 amino acid residues of the human immunodeficiency virus transmembrane protein (p41).
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PMID:FokI method of gene synthesis. 326 97

To evaluate the performance of a serological test for human immunodeficiency virus type 1 (HIV-1) infections based on the use of a recombinant envelope gene-derived protein as the antigen, we caused expression of a 1.4-kilobase fragment of HIV.DNA that codes for the complete gp41 transmembrane protein in an Escherichia coli expression vector and used Western blots (WB; immunoblots) prepared with recombinant material (pEX-41) to detect antibodies to HIV-1. This test detected all 339 sera which were positive by a combination of conventional serodiagnostic assays and produced no false-positive results with 311 negative samples. Also no false-positive results were obtained with 20 sera from systemic lupus erythematosus patients which had high titers of cross-reactive autoantibodies. In six cases, the pEX-41 WB proved to be more sensitive than individual assays applied on their own, and in five cases it was even more sensitive than a combination of conventional assays. We tested 221 sera in both our pEX-41 WB and a commercially available recombinant enzyme immunoassay (EIA [Abbott]). The results were identical in 188 cases. A total of 27 sera containing antibodies to gp41 as demonstrated in the pEX-41 WB, as well as the Abbott recombinant EIA, had no antibodies to the recombinant core antigen as measured in the Abbott EIA. However, 25 of these sera did stain the 24-kilodalton band on a WB with purified virus. Six sera that were positive in all of the conventional confirmatory assays and reacted strongly with the pEX-41 WB did not recognize the surface antigen used in the Abbott recombinant EIA. We conclude that the use of WB prepared with recombinant-derived p41 offers a very sensitive and specific method to detect antibodies to HIV.
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PMID:Comparison of Western blot (immunoblot) based on recombinant-derived p41 with conventional tests for serodiagnosis of human immunodeficiency virus infections. 327 88

Diagnosis of infection with the human immunodeficiency virus (HIV) relies on the demonstration of antibody to this virus. Occasionally, the combined analysis of sera using ELISA and western blot reveals false-positive results. We have compared a newly developed test to detect antibodies to the core (anti-p24) and surface (anti-p41) proteins of HIV with the established tests described above. Anti-p24 and anti-p41 were negative in three individuals positive for anti-HIV by ELISA and immunoblot; they had a low risk to acquire HIV infection and were clinically and immunologically normal and suspected false positive previously. In 62 individuals at risk, anti-p41 was always positive while anti-p24 was negative in 24/62 individuals including all but one patient with AIDS. The data indicate that this new test may replace the western blot as a reliable, widely available, and standardized confirmatory assay. In addition, preliminary evidence needs to be confirmed that quantitative analysis of anti-p24 might be of prognostic value in the course of HIV infection.
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PMID:Demonstration of antibodies to the surface (anti-p41) and core proteins (anti-p24) of the human immunodeficiency virus (HIV) in individuals positive for anti-HIV. 349 88

The purpose of this study was to characterize antigenic determinants on structural polypeptides of human immunodeficiency virus type 2 (HIV-2ben). Therefore, three HIV-2-specific monoclonal antibodies (mAbs) against the p24 core protein (gag) and one mAb against the gp130 envelope glycoprotein (env) were produced. In addition to p24 the anti-core mAbs recognized the primary translation product of the viral gag gene p55 and an intermediate cleavage product p41. Core mAbs cross-reacted with another HIV-2 isolate (HIV-2rod), and several simian immunodeficiency viruses (SIVagm TYO7 and SIVmac), but not with SIVmnd and the HIV-1 isolates investigated (HIV-1han and HIV-1lai). The env mAb cross-reacted with HIV-2rod and SIVmac but not with SIVagm, SIVmnd or HIV-1. In competition assays and with epitope mapping possible binding sites for the mAbs were identified. The processing of HIV-2 core proteins is compared in retrovirus-infected T cell lines and during the expression by recombinant vaccinia virus. Finally, the mAb XIV DC10 which recognized a highly conserved epitope could be useful for an assay to detect HIV-1 and HIV-2 simultaneously. II D8 is the first mAb raised against HIV-2 env glycoprotein.
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PMID:Generation, characterization and cross-reactivities of monoclonal antibodies against the p24 core protein and the gp130 envelope glycoprotein of HIV-2ben. 769 60

Productive, spreading infection of peripheral blood lymphocytes (PBL) with human immunodeficiency virus type 1 (HIV-1) requires the viral protein Vif. To study the requirement for vif in this system, we infected PBL with a phenotypically complemented HIV-1 clone mutated in vif. Progeny virus was produced which was noninfectious in PBL but replicated in SupT1 cells. Analysis of metabolically labeled proteins of sedimentable extracellular particles made in PBL by radioimmunoprecipitation with either serum from a patient with AIDS or a monoclonal antibody reactive with HIV-1 Gag proteins revealed that vif-negative but not wild-type particles carry higher levels of p55, p41, and p38 Gag-specific proteins compared with those of p24. Similar results were obtained with sucrose-purified virions. Our data indicate that vif plays a role in Gag protein processing or in incorporation of processed Gag products into mature virions. The presence of unprocessed precursor Gag polyprotein (Pr55gag) and other Gag processing intermediates in PBL-derived vif-negative extracellular particles may contribute to the reduced infectivity of this virus.
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PMID:Aberrant Gag protein composition of a human immunodeficiency virus type 1 vif mutant produced in primary lymphocytes. 776 28

To define virologic and immunologic differences in patients with acute symptomatic and asymptomatic primary human immunodeficiency virus type 1 (HIV-1) infection, sequential plasma specimens were obtained longitudinally for 1-2 years postseroconversion from subjects with well-documented time of seroconversion. Thirteen of them had an acute symptomatic primary infection, eight subjects had asymptomatic primary infection and long-term follow-up, and 27 had asymptomatic seroconversion and short-term follow-up. Quantitative plasma HIV-1 RNA levels, CD4+ lymphocyte counts, and levels of antibodies to gp120, p66, p41, p31, p24, and p17 were measured. At the time of seroconversion, there was no significant difference in HIV-1 RNA levels and CD4+ counts between symptomatic (n = 13) and asymptomatic (n = 27) subjects. Subsequently, however, establishment of low levels of plasma HIV-1 RNA was seen significantly more frequently in asymptomatic (n = 8) than in symptomatic (n = 13) primary infection; this correlated with higher levels of some (anti-gp120 and anti-p31) anti-HIV-1 antibodies and a slower decline in CD4+ lymphocyte counts. These results indicate that immunologic control of viremia early after infection may be a critical determinant to subsequent clinical course of HIV-1 infection. They also suggest that persons with acute symptomatic primary infection may generally progress to having acquired immune deficiency syndrome (AIDS) more rapidly than people with low-grade symptoms or asymptomatic primary infection.
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PMID:Virologic and immunologic characterization of symptomatic and asymptomatic primary HIV-1 infection. 778 30

In a cohort of infants born to human immunodeficiency virus type 1 (HIV-1)-infected mothers, changes in the levels of HIV-1 specific antibodies were measured during the first year of life. In uninfected children, the level of antibodies to six HIV-1 antigens (gp120, p66, p41, p31, p24, and p17) decreased continuously until becoming negative. In contrast, rising levels of one or more specific antibodies were detected in 9 of 12 infected children at a median age of 6 months. At 1 year of age, 8 infants were still asymptomatic and classified as P-1. All had serologic profiles consistent with de novo specific antibody production. In contrast, among the 4 infants who had early disease (class P-2), 3 had no significant rise in antibody to HIV-1. These results indicate that poor immune response, which could result from early infection of the infant, is often associated with rapid clinical progression.
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PMID:Ontogeny of the humoral immune response to human immunodeficiency virus type 1 in infants. 833 66

Viral protein U (Vpu) is an 81 amino acid phosphoprotein found in human immunodeficiency virus type 1 (HIV-1)-infected cells. One function of Vpu is to enhance the release of virus particles from the plasma membrane in infected cells. Using subcellular fractionation, we observed that Vpu promotes the targeting of Pr55 Gag to the plasma membrane, the site of viral assembly. Deletions of Pr55, which removed most of the N-terminal matrix domain (p39) or the C-terminal domains of nucleocapsid and p6 (p41), still allowed for virus-like particle production. Moreover, the release of these particles remained Vpu-responsive. The N-terminal matrix (MA) domain of Gag, which contains its membrane-binding domain, is sufficient for Vpu-mediated enhanced release into the supernatant. Furthermore, a MA-GFP fusion protein showed enhanced membrane binding in the presence of Vpu. This demonstrates that Vpu action may be mediated by allowing Gag, specifically the N-terminal matrix domain, to efficiently associate with the plasma membrane. Thus MA appears sufficient but not necessary for Vpu-mediated enhanced particle release.
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PMID:The N-terminal matrix domain of HIV-1 Gag is sufficient but not necessary for viral protein U-mediated enhancement of particle release through a membrane-targeting mechanism. 1075 9

Anti -human immunodeficiency virus (HIV) type 1 antibodies in 242 pregnant women and 238 infants were measured at birth and at 1, 2, 4, and 6 months after birth, to estimate their association with perinatal transmission and infant disease progression. Maternal anti-p24 (P=.01) and anti-gp120 (P=.04) antibodies were inversely associated with vertical transmission rates, independent of maternal percentage of CD4 cells, hard drug use, duration of ruptured membranes, serum albumin levels, serum vitamin A levels, and quantitative HIV-1 peripheral mononuclear blood cell culture, but not with maternal plasma immune complex dissociated p24 or HIV-1 RNA copy number, both of which were highly correlated with antibodies. From ages 1-2 months, anti-gp120, -gp41, -p31, and -p66 decayed to a greater extent in infected than in uninfected infants. Infected infants produced anti-p24 antibody by age 2 months, anti-p17 by 4 months, and anti-p41 and anti-gp120 by 6 months. As early as birth, infants with rapid disease progression had lower levels of anti-p24 than did infants whose disease did not rapidly progress, but not independently of HIV-1 RNA levels.
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PMID:Human immunodeficiency virus (HIV) type 1 antibodies in perinatal HIV-1 infection: association with human HIV-1 transmission, infection, and disease progression. For the Women and Infants Transmission Study. 1097 26


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