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)

The proportion of nucleated splenocytes bearing B-lymphocyte markers B220, surface IgM (sIgM) and sIgD, as well as the T-lymphocyte markers Thy 1.2, CD5, CD8a and CD4 were quantitated by flow cytometric analysis (FACS) throughout postpartum development in the A/J mouse. Full expression of B lymphocyte markers was achieved much sooner than expression of T lymphocyte markers. This was especially true for B220, which was found on 8% of all splenocytes at day 5 and reached adult levels (47-50%) by weaning at day 22. Expression of sIgM and sIgD were 13% and 9%, respectively, of all splenocytes at day 5 with mature levels not expressed until day 35 postpartum (approximately 36% of cells were positive for these markers). T lymphocyte markers, on the other hand, did not reach full expression until sexual maturity. For example, Thy 1.2 expression was 8% on day 5 and did not reach mature levels (28-30%) until day 56. CD5 closely paralleled Thy 1.2 expression rising from only 2% on day 5 to 27% by day 56. Likewise, CD8a and CD4 marker development paralleled one another with CD8a rising from 1% on day 5 to 10% by day 56 and CD4 rising from 5% on day 5 to 19% by day 56. These data demonstrate the variability in the time of appearance and rate of maturation of the various lymphocyte cell surface markers during postpartum development. They also serve as a reference to identify alterations in lymphocyte development created by immunodeficiency diseases.
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PMID:Flow cytometric analysis of the expression of murine B and T surface markers from birth to adulthood. 134 52

The role of carbohydrates in the immunogenicity of human immunodeficiency virus type 1 (HIV-1) glycoproteins (gp160 and gp120) remains poorly understood. We have analyzed the specificity and neutralizing capacity of antibodies raised against native gp160 or against gp160 deglycosylated by either endo F-N glycanase, neuraminidase, or alpha-mannosidase. Rabbits immunized with these immunogens produced antibodies that recognized recombinant gp160 (rgp160) from HIV-1 in a radioimmunoassay and in an enzyme-linked immunosorbent assay. Antibodies elicited by the different forms of deglycosylated gp160 were analyzed for their reactivity against a panel of synthetic peptides. Compared with anti-native gp160 antisera, serum reactivity to most peptides remained unchanged, or it could increase (peptide P41) or decrease. Only antibodies raised against mannosidase-treated gp160 failed to react with a synthetic peptide (peptide P29) within the V3 loop of gp120. Rabbits immunized with desialylated rgp160 generated antibodies which recognized not only rgp160 from HIV-1 but also rgp140 from HIV-2 at high titers. Although all antisera produced against glycosylated or deglycosylated rgp160 could prevent HIV-1 binding to CD4-positive cells in vitro, only antibodies raised against native or desialylated gp160 neutralized HIV-1 infectivity and inhibited syncytium formation between HIV-1-infected cells and noninfected CD4-positive cells, whereas antibodies raised against alpha-mannosidase-treated gp160 inhibited neither virus replication nor syncytium formation. These findings indicate that the carbohydrate moieties of gp160 can modulate the specificity and the protective efficiency of the antibody response to the molecule.
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PMID:Influence of carbohydrate moieties on the immunogenicity of human immunodeficiency virus type 1 recombinant gp160. 134 97

To assess the hypothesis that the human immunodeficiency virus (HIV) might mimic major histocompatibility complex (MHC) allodeterminants and interact with T-cell receptors (TCRs) of alloreactive T-cells, we have done a preliminary analysis of the range of alpha beta TCR gene products in 16 HIV-1-seropositive individuals with normal CD4 counts and in 16 healthy HIV-1-negative controls. Using a panel of monoclonal antibodies with a two-colour direct immunofluorescence method, we found a significant increase in the expression of the V beta 5.3 subfamily in the HIV-positive patient group compared with controls (p less than 0.01). Selected increase in expression of V beta sequences has been described in various autoimmune conditions and our findings raise the possibility that the immunopathological damage from HIV infection may be due to the induction of autoreactivity. If HIV does mimic MHC II, the normal immune response to the virus could represent an autoimmune process similar to graft-versus-host disease.
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PMID:T-cell receptor variable gene products and early HIV-1 infection. 135 71

Syncytia or multinucleated giant-cell formation is one of the major cytopathic effects induced by human immunodeficiency virus (HIV) infection. Cell fusion results from the strong interaction of CD4 molecules on the surface of the uninfected T cells and gp120, an external envelope glycoprotein of HIV on the infected T cells. We studied the production of HIV in fusion cells between MOLT-4 and virus-infected MOLT-4/HIV cells and found that HIV production was enhanced up to three- to fivefold, which showed a good correlation with the appearance and extent of syncytia formation. Blocking the fusion by monoclonal antibody against a binding epitope of CD4 molecule to gp120 decreased the HIV production significantly. Enhancement of HIV production was observed by more than five-fold in comparison with chronically infected cells, which were fusion free 20 hr postcocultivation. Electron microscopic observation also showed the presence of abundant HIV particles inside the fused cells and on the outer surface. AZT blocked the HIV augmentation of fused cells in coculture completely. Southern blot analysis revealed that both integrated and unintegrated HIV DNA were highly accumulated in fusion cells, as compared with fusion-free MOLT-4/HIV cells. Among unintegrated DNA, circular and linear DNA were accumulated to a similar degree. Northern blot hybridization showed that rapid enhancement of all three species of HIV-specific RNA containing genomic (9.2 kb) and subgenomic (4.3 and 1.9 kb) RNAs were found 20 hr postinfection in fusion cells. These data suggest that syncytia formation is an extremely active infection process of HIV, by which multiple rounds of reinfection might take place.
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PMID:Increased production of human immunodeficiency virus (HIV) in HIV-induced syncytia formation: an efficient infection process. 134 63

Thrombocytopenia is a known complication of human immunodeficiency virus Type-1 (HIV-1) infection, and more data need to be collected on its frequency, severity, and clinical sequelae. We determined the frequency of thrombocytopenia and its relationship to other HIV infection characteristics from a review of records of 1004 HIV-infected patients attending two outpatient clinics in Washington, D.C. The self-reported sources of HIV-1 exposure were male homosexual activity (68%), bisexual activity (10%), heterosexual activity (6%), and intravenous drug use (15%). Fifty-nine percent of the individuals were white, 37% were black and 94% were male. Fifteen percent had AIDS. Thrombocytopenia occurred more frequently in subjects with AIDS (21.2%) than in HIV-infected individuals who did not fit clinical criteria for AIDS (9.2%) (p less than 0.001). Patients with few CD4-positive cells and an advanced stage of disease were more likely to have low platelet counts: 30% with an absolute CD4 cell count lower than 200/mm3 vs 8% with CD4 counts between 200 and 500 (p less than 0.00001), and 18.5% with Stage IV disease compared to 7.6% in Stage II (p less than 0.001) had platelet counts less than 150,000/mm3. Thrombocytopenia was more frequent in white males and older subjects. Although subjects infected by heterosexual exposure had a lower frequency of thrombocytopenia, intravenous drug users and homosexual men exhibited similar frequencies of thrombocytopenia. Of all subjects with platelet counts less than 50,000/mm3, 40% reported bleeding and 1 died of an intracranial hemorrhage. Thrombocytopenia occurs frequently in HIV-infected people, primarily in those with AIDS, low CD4 cell numbers, and advanced stages of diseases.
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PMID:Epidemiology of thrombocytopenia in HIV infection. 850 Jun 8

We examined the association of three serum immune markers with CD4 cell counts in a large cohort of i.v. drug users with and without human immunodeficiency virus (HIV) infection. Levels of beta 2-microglobulin and neopterin were significantly elevated in HIV-infected subjects and increased in association with decline in CD4 cell counts (all p less than 0.001). Serum IgA levels in HIV-seropositive individuals were significantly elevated only when the CD4 cell count was less than 200/microliters (p less than 0.001). After controlling for HIV status and CD4 count, recent history of hepatitis was associated with significantly higher beta 2-microglobulin (p = 0.028) and marginally higher neopterin (p = 0.052) levels. There was no association of race, gender, or drug use patterns with levels of serum immune markers after controlling for HIV status and CD4 count. These data indicate that immune activation is coupled with immunosuppression in HIV-infected i.v. drug users. In addition, beta 2-microglobulin and neopterin levels are elevated in persons with a recent history of hepatitis but not in those with recent non-AIDS-defining bacterial infections. Markers of immune activation do not vary by race, gender, or drug use patterns among i.v. drug users.
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PMID:Immune serum markers and CD4 cell counts in HIV-infected intravenous drug users. 136 May 38

When neonatal FVB/N mice were inoculated with ts1, a temperature-sensitive mutant of Moloney murine leukemia virus TB, they developed a progressive bilateral hindlimb paralysis and immunodeficiency leading to death 4 to 6 weeks after inoculation. T lymphocytes have been shown to be primarily responsible for this ts1-induced syndrome. Here we compare the role played by each subset of T lymphocytes, i.e., CD4+ and CD8+ T cells, in disease development. Mice were depleted of a specific subset for the first 10 days of their lives by using either anti-CD4 or anti-CD8 monoclonal antibodies in vivo. Disease development in these mice was then monitored. Depletion of CD4+ T cells significantly attenuated the ts1-induced syndrome: virus replication was decreased, disease latency was extended, and death was prevented in 60% of the mice. Similar treatment with anti-CD8 antibody had almost no effect on disease progression. However, when depletion was begun 2 weeks after neonatal ts1 inoculation, CD4+ T cell depletion did not affect disease development. ts1 infected CD4+ and CD8+ T lymphocytes equally well in vivo, as shown by flow cytometric analysis, but virus replication was restricted primarily to the CD4+ subset of T cells, as found by in vitro assay. Hence, CD4+ T lymphocytes play an important role in the development of ts1-induced paralysis and immunodeficiency. The mechanism of this CD4+ T-cell-mediated disease production by ts1 is not clear; however, increased replication of ts1 in the CD4+ T cells, especially in the early stages of the disease, seems to play a crucial role.
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PMID:ts1, a temperature-sensitive mutant of Moloney murine leukemia virus TB, can infect both CD4+ and CD8+ T cells but requires CD4+ T cells in order to cause paralysis and immunodeficiency. 134 44

We analysed the expression of lymphocyte function-associated antigen LFA-1 on the cell surface of peripheral blood lymphocytes, monocytes and granulocytes from 20 children with Down's syndrome. No differences in LFA-1 expression was found within monocytes or granulocytes from either normal or Down's syndrome children; however, a clear-cut difference was observed on lymphoid cells. Both normal and Down's syndrome lymphocytes displayed a bimodal pattern of LFA-1 staining by flow cytometry, with a predominance of cells with low expression in normal population, and an increased proportion of lymphocytes with high level of LFA-1 expression in Down's syndrome children. This difference correlates well with the abnormal proportion of T cell subsets and inversion of CD4/CD8 observed in a majority of our cases, and therefore, it could merely reflect the increase of certain T cell subsets normally expressing higher number of LFA-1 molecules. Taken together, our results do not support an abnormally increased expression of leucocytes integrins in trisomy 21 cells, and raise some doubt about the suggested role of the abnormal cellular expression of LFA-1 in the pathogensis of secondary immunodeficiency associated to Down's syndrome.
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PMID:Differential expression of lymphocyte function-associated antigen (LFA-1) on peripheral blood leucocytes from individuals with Down's syndrome. 134 67

To investigate its use as a marker of disease severity, serum soluble CD4 (sCD4) was measured by ELISA in patients with human immunodeficiency virus (HIV) infection. Levels of sCD4 were higher in patients than in controls (P less than .001) but did not increase with disease severity. sCD4 release per CD4 lymphocyte showed a linear increase with disease severity and performed as well as beta 2-microglobulin, a widely used marker. To study the role of sCD4 in the pathogenesis of HIV infection, an ELISA to detect sCD4 complexed with glycoprotein 120 (gp120) HIV envelope protein was developed. Preformed sCD4-gp120 complexes were not detectable in patient serum, but addition of recombinant gp120 showed that circulating sCD4 is capable of binding HIV envelope proteins. This study indicates that the sCD4-to-CD4 lymphocyte ratio increases linearly with disease severity and may be a useful marker of CD4 lymphocyte damage. In addition, serum sCD4 can bind viral particles, which may have implications for the use of recombinant sCD4 as a therapy in HIV infection.
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PMID:Naturally occurring soluble CD4 in patients with human immunodeficiency virus infection. 134 32

Children born to women known to be infected with human immunodeficiency virus type 1 (HIV-1) before delivery were followed prospectively from birth in nineteen European centres. This analysis, encompassing the period end-December, 1984, to beginning-August, 1991, focuses on risk factors for mother-to-child transmission of HIV-1 infection. Rate of vertical transmission, based on 721 children born to 701 mothers more than 18 months before the time of analysis, was 14.4% (95% Cl 12.0-17.1%). Transmission was associated with maternal p24-antigenaemia and a CD4 count of less than 700/microliters. In a multivariate analysis, odds ratios of transmission were: 2.25 (95% Cl 0.97-5.23) in breastfed children vs never-breastfed children; 3.80 (1.62-8.91) in children born before 34 weeks' gestation; and 0.56 (0.30-1.04) in children delivered by caesarean section. Transmission was higher with vaginal deliveries in which episiotomy, scalp electrodes, forceps, or vacuum extractors were used, but only in centres where these procedures were not routine. On the basis of these results, HIV-infected women contemplating pregnancy should be counselled according to their immunological findings and, if they have p24-antigenaemia or a low CD4 count, warned of an increased risk of viral transmission. Caesarean deliveries may have a protective effect, although it is premature to recommend routine operative delivery. The mechanism for the higher infection rate in children born before 34 weeks' gestation is unclear, but could reflect inadequate passive or active immunity at that age, combined with substantial transmission during labour or delivery. The balance of evidence suggests that mothers with established infection can transmit HIV infection through breastmilk, although the relative importance of this route remains to be defined.
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PMID:Risk factors for mother-to-child transmission of HIV-1. 135 93


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