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)

T cell stimulation by the human immunodeficiency virus 1 gp160-derived peptide p18 presented by H-2Dd class I major histocompatibility complex molecules in a cell-free system was found to require proteolytic cleavage. This extracellular processing was mediated by peptidases present in fetal calf serum. In vitro processing of p18 resulted in a distinct reverse phase high performance liquid chromatography profile, from which a biologically active product was isolated and sequenced. This peptide processing can be specifically blocked by the angiotensin-1 converting enzyme (ACE) inhibitor captopril, and can occur by exposing p18 to purified ACE. The ability of naturally occurring extracellular proteases to convert inactive peptides to T cell antigens has important implications for understanding cytotoxic T lymphocyte responses in vivo, and for rational peptide vaccine design.
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PMID:Serum angiotensin-1 converting enzyme activity processes a human immunodeficiency virus 1 gp160 peptide for presentation by major histocompatibility complex class I molecules. 131 30

Five monoclonal antibodies (MAbs) were raised against the gag proteins of simian immunodeficiency virus (SIV) from African green monkey (SIVagmTYO-7). Two MAbs reacted with the matrix protein p17 and the other three with the core protein p24. Studies on the cross-reactivity of the MAbs revealed that the anti-p24 MAbs detected an epitope shared by the viruses belonging to the human immunodeficiency virus type 2 (HIV-2)/SIVmac group and SIVagmTYO-7 and SIVagmTYO-5. The anti-p17 MAbs recognized an epitope present on all these viruses and on SIVagmTYO-1, HIV-1 and SIVmnd. This finding demonstrates for the first time that the matrix protein, p17 or p18, respectively, of all nine HIV and SIV isolates tested in this study expresses at least one conserved immunogenic epitope recognized serologically. By using synthetic peptides, this epitope was identified at the N terminus of p17. Furthermore, this epitope was analysed by multiple sequence alignments of the peptide with homologous sequences of HIV and SIV p17.
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PMID:Identification of a gag protein epitope conserved among all four groups of primate immunodeficiency viruses by using monoclonal antibodies. 138 99

The effectiveness and security of azidothymidine (AZT) in the treatment of patients with infection by the human immunodeficiency virus (HIV) and persistent generalized adenopathies (PGA), were assessed. Thirty six patients with HIV infection and PGA participate in the study. Eighteen were treated with AZT and the other 18 were included in the control group, since they did not accept the treatment. Both groups were homogeneous with respect to their clinical, immunological and virological characteristics. A common study protocol was used and the clinical, immunological and virological effectiveness was assessed. Lymphocyte subpopulations were quantified by flow cytometry, viral antigens were determined by sandwich-type ELISA and antibodies against viral proteins (anti-gp120, anti-gp160, anti-gp41, anti-gp24 and anti-p18) were detected by Western blot. Naranjo and Busto's algorithm was used for the causality of adverse effects. We did not observe any significant differences regarding the presence of infection and the evolution of AIDS in both groups. A positive response to thrombocytopenia was observed, more evident in patients under low doses of AZT. The small initial transitory improvement of the immunological parameters was not statistically significant. The viral antigen was not modified by the treatment. With respect to the behaviour of the several antibodies studied, no differences were observed. The initial doses of AZT had to be modified in 44% of patients due to their hematological toxicity, more frequent in the first stages of the treatment. In two patients, the treatment had to be finally discontinued due to severe neutropenia. 25% of patients showed mild to moderate gastrointestinal manifestations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Azidothymidine in the treatment of patients with human immunodeficiency virus infection and persistent generalized adenopathies]. 146

The processing of the human immunodeficiency virus (HIV) gag and gag-pol precursor proteins by the virus-encoded protease is an essential step in maturation of infectious virus particles. Like most retroviral proteases, the HIV protease belongs to the aspartyl-protease family and can be inhibited by specific inhibitors. Twenty-four synthetic peptides known to be inhibitors of human renin were tested for inhibition of HIV replication in tissue cultures. One of them, a synthetic peptide analogue, SR41476, which has been shown to be a specific inhibitor of purified recombinant HIV1 protease in vitro, totally blocked infection with different isolates including the HIV1 LAV prototype, the highly cytopathic Zairian isolate HIV1 NDK, and HIV2 ROD, both in primary blood lymphocytes (PBL) and in the lymphoid cell lines MT4 and CEM, for at least 3 weeks. It also significantly reduced virus replication in chronically infected CEM cells, without any effect on cell proliferation. Radioimmunoprecipitation assay revealed that the inhibitor blocked processing of polyprotein precursors p55 gag and p40 gag into a mature form of gag proteins, p25 and p18. Synthetic peptide analogue SR 41476, when added before infection, efficiently inhibited formation of HIV DNA provirus and successfully suppressed synthesis of HIV-specific proteins. These results imply that the HIV protease inhibitor not only inhibited virus maturation in the late phase of the HIV replication cycle, but also interfered in the early phase, before the provirus was formed. This mechanism of antiviral activity provides new possibilities and strategies for AIDS chemotherapy.
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PMID:Inhibition of HIV by an anti-HIV protease synthetic peptide blocks an early step of viral replication. 148 Aug 23

This study analyzes the correlation of basic laboratory test results with clinical outcome in 94 children with perinatally acquired human immunodeficiency virus 1 infection who did not receive zidovudine during the study period of 1983 to 1988. Two life-threatening conditions highly correlated with survival, opportunistic infection and severe encephalopathy, were the end points of the study. At a median age of 25 months 30 (32%) of the 94 children had developed such conditions (Group I), and their survival at 3 years of age was 48% (95% confidence interval, 24 to 72%), contrasting with the 97% survival rate (95% confidence interval, 94 to 100%) of the remaining 64 (68%) children who had not developed such conditions by age 25 months. (Group II). Compared with children in Group II, children with life-threatening complications were more likely at the onset of symptoms to be younger and have a lower CD4 count, an impaired in vitro lymphocytic proliferation and a lack of p18 or p25 antibodies in the Western blot profile and, during the progression of the disease, a negative slope of the subsequent CD4 counts. These results highlight the need for an early diagnosis of the human immunodeficiency virus 1 infection in children and demonstrate that it is possible to determine the prognosis of their disease as early as in the first year of life.
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PMID:Natural history of human immunodeficiency virus type 1 infection in children: prognostic value of laboratory tests on the bimodal progression of the disease. 152 73

Only "fair" agreement has been shown between the Abbott and DuPont enzyme linked immunosorbent assays when used for the detection of human immunodeficiency virus (HIV) antigen in serum samples from asymptomatic HIV antibody positive homosexual men. To investigate the discrepancies between the two ELISA results, further experiments were performed. The rabbit detector antibody solutions of both tests were western blotted and showed that the DuPont test was specific for p24; the Abbott detector antibody had bands for p18, p41-43, gp120 as well as p24. By using dilutions of a known amount of HIV antigen, the Abbott test could detect 20 pg/ml p24; the DuPont test could detect 30 pg/ml p24. The DuPont test was also more sensitive than the Abbott test at detecting a synthetic 104mer peptide of p24. Within the 104mer sequence two regions (294-318, 334-348 amino acids) inhibited the binding of the DuPont detector antibody, but no blocking was observed with the Abbott antibody. Although the Abbott test was slightly more sensitive at detecting HIV protein than the DuPont test, the major difference between the tests was in the molecular specificity, in that the Abbott test detected proteins other than p24. This may not be important for detecting antigen in cell culture, but it may affect the detection of antigenaemia in patients' sera.
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PMID:Molecular specificity of two commercial enzyme linked immunosorbent assays for human immunodeficiency virus antigens. 179 Dec 2

Sera from 124 persons in high risk groups were analyzed including homosexuals, blood recipients, and spouses or siblings from AIDS patients. In this study, 118 individuals had a positive ELISA for anti-HIV antibodies. Six persons had a complete immunodeficiency syndrome and a negative ELISA test. In the Western blot, 111 sera were positive, four negative, and nine scored indeterminate; four of the latter converted to positive when retested three months later. Antibodies present in the positive sera were directed against the HIV gp 41 kD in 100% of the cases and against the gp 120 kD in 82%. Frequency of recognition of p55 kD was 96% but p18 kD was only 42%.
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PMID:[Immunoelectroblotting in Mexican subjects at high risk for infection with human immunodeficiency virus (HIV)]. 181 69

To better define the clinical and biological evolution of infants after vertical human immunodeficiency virus type 1 infection, we analyzed 94 consecutive infected patients followed up after their first clinical symptoms. The expression of clinical symptoms and biological abnormalities followed a bimodal distribution, some patients having an early and severe disease and the others having a slowly progressive one. One third of our patients suffered from early onset of opportunistic infection (OI). These patients had a significantly higher incidence of severe encephalopathy compared with patients without OI. The rate of survival at 3 years was 48% +/- 24%. In contrast, the patients without early OI or severe encephalopathy had a probability of survival at 3 years of 97% +/- 3%. This probability was not modified by the occurrence of bacterial infection or lymphoid interstitial pneumonitis. Lymphoid interstitial pneumonitis occurred at a mean age of 29 months, significantly later than OI or severe encephalopathy. Laboratory results at initial examination were correlated with clinical symptoms. Thus, when the number of CD4 lymphocytes was less than 500/mm3, children suffered more frequently from life-threatening symptoms (OI and severe encephalopathy): 15 of 22 vs 14 of 69. The same was true when the lymphocytes did not proliferate after antigenic stimulation, when anti-p18 and/or anti-p25 antibodies were absent in the serum, and when p24 antigen was detected in serum. Finally, severe encephalopathy was associated with low anti-human immunodeficiency virus cerebrospinal fluid antibody titer, whereas 88% of patients with moderate or no encephalopathy had signs of intrathecal anti-human immunodeficiency virus antibody synthesis. In conclusion, a subgroup of patients expressed very early signs of severe immunodeficiency and encephalopathy, whereas the majority of patients had a longer survival and less severe clinical symptoms during their first years of life than previously thought.
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PMID:Longitudinal study of 94 symptomatic infants with perinatally acquired human immunodeficiency virus infection. Evidence for a bimodal expression of clinical and biological symptoms. 166 56

We have characterized a novel 28-kilodalton protein, p28tev, detected in human immunodeficiency virus type 1-infected cells. tev is recognized by both tat and rev monospecific antibodies. tev is initiated at the tat AUG and contains the first exon of tat at its amino terminus, a small portion of env in the middle, and the second exon of rev at its carboxy terminus. A cDNA clone producing tev was cloned and expressed in human cells. Sequence analysis revealed that the tev mRNA is generated by splicing to a novel exon located in the env region. This identifies a fourth class of multiply spliced human immunodeficiency virus mRNAs, produced in infected and transfected cells. tev is regulated during the virus life cycle similarly to the other regulatory proteins, tat, rev, and nef, and displays both tat and rev activities in functional assays. Since tev contains important functional domains of tat and rev and is produced very early after transfection, it may be an important regulator in the initial phase of virus expression. Another rev-related protein, p18(6)Drev, containing env and rev sequences, was characterized and was found not to have detectable rev activity.
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PMID:A novel human immunodeficiency virus type 1 protein, tev, shares sequences with tat, env, and rev proteins. 218 72

Reports of rare cases of suspected transmission of the human immunodeficiency virus (HIV) from mother to children by breast milk have been recently published. To study the factors that possibly limit HIV transmission through breast-feeding, milk samples obtained from 15 healthy, seropositive mothers and 4 seronegative control subjects were studied for the presence of anti-HIV antibodies. All samples from seropositive women contained IgG antibody against envelope glycoproteins gp160 and/or gp120, and 11 of 15 samples contained IgA antibodies against gp160. IgA antibodies against other viral antigens were more rarely recovered, except against the internal proteins of the virus, p18 and p25. The finding of IgA antibodies to HIV-1 in breast milk establishes that the virus elicits a local immune response in heterosexual, seropositive women. The role of local antibodies in the postnatal transmission of HIV remains to be determined.
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PMID:Antibodies to human immunodeficiency virus in the breast milk of healthy, seropositive women. 233 25


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