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)

Immunofluorescence and immunoblot assays were conducted on 488 sera from patients with AIDS and clinically healthy individuals at risk for infection by the human immunodeficiency virus. Of these, 360 contained antiviral antibodies, and nearly all reacted with the envelope precursor glycoprotein gp160. Sera from 103 individuals for whom a complete clinical history was available were evaluated in detail. Most sera recognized both the gp160 and the p55 gag precursor protein. Because these two antigens are found primarily in infected cells, the results suggest that this association makes them more immunogenic. A high prevalence of antibodies to the polymerase gene products (p65 and p31) and to a viral protein p48, which is not yet fully defined, was also noted. Many sera, particularly those from patients with Kaposi's sarcoma or Pneumocystis carinii pneumonia, lacked antibodies to both p25 and gp41. These antibody patterns could help predict the prognosis for virus-infected individuals.
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PMID:Patterns of antibody response in individuals infected with the human immunodeficiency virus. 354 16

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

Although human immunodeficiency virus (HIV) infection is progressive, the rate of decline in CD4+ lymphocyte counts varies. The role of immune system components in limiting HIV infection has yet to be defined, but a previous report on the U.S. Navy HIV Seropositive Cohort reported that strong reactivity in the anti-p55 (core precursor), p24 (core) and p53 (reverse transcriptase) Western blot bands was associated with higher CD4+ lymphocyte counts at the first clinical evaluation for HIV. The previous report examined the cross-sectional association between Western blot banding patterns and initial CD4+ lymphocyte counts. This report examines the association between these banding patterns in individuals who progressed rapidly as compared with patterns of patients who did not, based on their trends in repeated CD4+ lymphocyte counts as a marker of progression. Rapid and slower progressors were identified from a cohort of 3414 Navy and Marine Corps personnel who had a first positive HIV Western blot during 1986-1991. For purposes of this study, rapid progressors were defined as individuals whose CD4+ lymphocyte counts declined to < 500 cells/mm3 within 1 year of seroconversion. A total of 325 individuals met these criteria. A comparison group of 63 slower progressors also was identified; this group consisted of those whose CD4+ lymphocyte counts remained at > or = 500 cells/mm3 for a minimum of 5 years of follow-up after their first positive Western blot. Rapid progressors were slightly younger than slower progressors and were more likely to be never married but did not differ significantly from slower progressors in race or sex. Rapid progressors had weaker reactivity in the anti-p55 core precursor (P < 0.0001), p15 core (P < 0.01), gp41 transmembrane (P < 0.01) and p31 endonuclease (P < 0.05) bands on the Western blot. The odds ratio for rapid progressor status associated with weak or absent reactivity was 7.8 in the anti-p55 band and ranged from 2.0 to 3.2 in the anti-p31, p15, and gp41 bands. These associations remained significant after adjustment for age, race, and sex. The p55 association persisted in repeated Western blots during routine clinical evaluation during a period of 5 years after the first positive Western blot. It was concluded that several possible explanations may account for the weaker reactivity of rapid progressors: (i) weak anti-p55 reactivity might have been a marker of early immune system damage; (ii) high concentrations of p55 or related proteins in the serum may have bound the available anti-p55 antibodies in rapid progressors, making them difficult to identify on the Western blot; or (iii) lack of anti-p55, p15, gp41, or p31 reactivity might have allowed more rapid progression.
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PMID:Western blot banding patterns of HIV rapid progressors in the U.S. Navy Seropositive Cohort: implications for vaccine development. Navy Retroviral Working Group. 887 45

Syphilis has once again become a public health issue with the advent of human immunodeficiency virus (HIV) infection. We report a 28-year-old Chinese man with recently acquired HIV infection together with early neurosyphilis. His presentation of acute mononucleosis-like syndrome, lymphadenopathy, aseptic meningitis, positive central nervous syndrome and reactive Venereal Disease Research Laboratory test in his cerebrospinal fluid helped to reach the diagnosis. Paired serum Western blot tests for HIV infection performed 1 month apart revealed either a new appearance or an increasing intensity of bands for p17, p24, p31, gp41, p52, p55, p68, gp120 and gp160 suggesting recently acquired HIV infection. The lymphadenopathy disappeared spontaneously and the neurosyphilis responded well to 14 days of penicillin G therapy. The Western blot pattern, clinical course, laboratory data, and therapeutic response indicated that the acute retroviral syndrome and early central nervous system involvement caused by Treponema pallidum occurred concomitantly.
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PMID:Concomitant human immunodeficiency virus infection and syphilitic meningitis. 906 8

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

The serodiagnosis of human immunodeficiency virus (HIV) infection has widely been established by the screening test and the confirmatory test. At present, Western blot (WB) assay is mostly used as the confirmatory test. However, this method has the problem in that the sensitivity and the specificity are not enough. A new confirmatory test "CHIRON RIBA HIV-1/HIV-2 SIA" developed by Chiron Corporation uses an immunoblot enzyme immunoassay technique for detection of anti HIV-1 and/or HIV-2 antibodies. This assay employs four recombinant viral antigens (gp120, gp41, p24/p26 and p31) and a synthetic viral antigen (HIV-2 envelope peptide). The characteristic of this method is that the HIV-1 infection and the HIV-2 infection can be differentiated from each other. We therefore compared this SIA method with the WB1 assay for detection of anti HIV-1 antibodies and with the WB2 assay for detection of anti HIV-2 antibodies. Eighty samples from normal adults without HIV infection and known to be negative by three HIV screening tests, respectively, were tested by SIA, WB1 and WB2 assays. The negative rates (specificities) were 97.5%, 80.0% and 87.5% by the SIA, WB1 assay and WB2 assay, respectively. With forty samples from patients without HIV infection but known to be positive by at least one HIV screening test, the negative rates (specificities) were 97.5%, 72.5% and 85.5% by the SIA, WB1 assay and WB2 assay, respectively. The results indicated that the SIA method was more specific than two WB assays. Forty samples from patients with HIV-1 infection and known to be positive by three HIV screening tests, were tested by the SIA and WB1 assay. The positive rates (sensitivities) were 97.5% and 75.0% by the SIA and WB1 assay, respectively. With thirteen samples from patients with HIV-2 infection and known to be positive by three HIV screening test, the positive rates (sensitivities) were 100% and 92.3% by the SIA and WB1 assay, respectively. The results indicated that the SIA method was more sensitive than the WB1 assay. Three sets of sera, which were collected during seroconversion for HIV-1 antibody, were used to compare the positive readings by the SIA and WB1 assay. The SIA method indicated the positive readings earlier than the WB1 assay. The present findings indicated that the SIA method was more specific and sensitive than the WB assay, and would be useful as a confirmatory test.
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PMID:[Strip immunoblot assay (SIA) with recombinant antigens and synthetic peptide for detection of anti HIV-1 and HIV-2 antibodies]. 1142 86

The resistance of rats or mice to glutamate-induced toxicity depends on their ability to spontaneously manifest a T cell-dependent response to the insult. Survival of retinal ganglion cells (RGCs) exposed to glutamate in BALB/c SCID mice (a strain relatively resistant to glutamate toxicity) was significantly worse than in the wild type. In the susceptible C57BL/6J mouse strain, however, significantly more RGCs survived among SCID mutants than in the matched wild type. RGC survival in the SCID mutants of the two strains was similar. These results suggest 1) that immunodeficiency might be an advantage in strains incapable of spontaneously manifesting protective T cell-dependent immunity and 2) that B cells might be destructive in such cases. After exposure of RGCs to toxic glutamate concentrations in three variants of B cell-deficient C57BL/6J mice, namely muMT(-/-) (B cell knockout mice) and Ii(-/-) mice reconstituted with transgenically expressed low levels of Ii p31 isoforms (p31 mice) or Ii p41 isoforms (p41 mice), significantly more RGCs survived in these mice than in the wild type. The improved survival was diminished by replenishment of the B cell-deficient mice with B cells derived from the wild type. It thus seems that B cells have an adverse effect on neuronal recovery after injury, at least in a strain that is unable to spontaneously manifest a T cell-dependent protective mechanism. These findings have clear implications for the design of immune-based therapies for CNS injury.
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PMID:Severe immunodeficiency has opposite effects on neuronal survival in glutamate-susceptible and -resistant mice: adverse effect of B cells. 1221 98

We have generated a codon-optimized hGagp17p24-Polp51 plasmid DNA expressing the human immunodeficiency virus type 1 (HIV-1) Gag-Pol fusion protein that consists of clusters of highly conserved cytotoxic T lymphocyte (CTL) epitopes presented by multiple MHC class I alleles. In the hGagp17p24-Polp51 construct, the ribosomal frameshift site had been deleted together with the potentially immunosuppressive Gag nucleocapsid (p15) as well as Pol protease (p10) and integrase (p31). Analyses of the magnitude and breadth of cellular responses demonstrated that immunization of HLA-A2/K(b) transgenic mice with the hGagp17p24-Polp51 construct induced 2- to 5-fold higher CD8+ T-cell responses to Gag p17-, p24-, and Pol reverse transcriptase (RT)-specific CTL epitopes than the full-length hGag-PolDeltaFsDeltaPr counterpart. The increases were correlated with higher protection against challenge with recombinant vaccinia viruses (rVVs) expressing gag and pol gene products. Consistent with the profile of Gag- and Pol-specific CD8+ T cell responses, an elevated level of type 1 cytokine production was noted in p24- and RT-stimulated splenocyte cultures established from hGagp17p24-Polp51-immunized mice compared to responses induced with the hGag-PolDeltaFsDeltaPr vaccine. Sera of mice immunized with the hGagp17p24-Polp51 vaccine also exhibited an increased titer of p24- and RT-specific IgG2 antibody responses. The results from our studies provide insights into approaches for boosting the breadth of Gag- and Pol-specific immune responses.
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PMID:Clustered epitopes within the Gag-Pol fusion protein DNA vaccine enhance immune responses and protection against challenge with recombinant vaccinia viruses expressing HIV-1 Gag and Pol antigens. 1568 Apr 12


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