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)

Multiple biopsies taken from 76 European human immunodeficiency virus (HIV)-negative patients with primary cutaneous T-cell lymphoproliferations, including mycosis fungoides (MF), pleomorphic T-cell lymphoma (PMTCL), anaplastic large cell lymphoma (ALCL) and lymphomatoid papulosis (LyP) were investigated for the presence of Epstein-Barr virus (EBV) through a combined approach. Polymerase chain reaction (PCR) was employed for EBV-DNA detection, in situ hybridization (ISH) for cellular localization of EBV-encoded nuclear RNAs (EBER1 and EBER2) and immediate early Bam H-fragment; lower frame (BHLF) RNA, and immunohistology (IH) for the identification of EBV-encoded latent membrane protein 1 (LMP1) and of nuclear antigen (EBNA) 2 expression. EBV-DNA was detectable by PCR in 15 of 76 cases (19.7%). EBER-ISH combined with IH identified a variable, usually very low, number of infected neoplastic cells in only seven of the 15 EBV-DNA-harbouring cases. This discrepancy between the results obtained with PCR and ISH is apparently caused by the low number of the infected cells per tissue section. The PMTCL entity produced the greatest number of positive cases, whilst ALCL and LyP cases were almost constantly devoid of the virus. BHLF transcripts were not detectable in any case, nor did any of the EBER-positive cells show an LMP1 or EBNA2 expression. These data show that primary cutaneous T-cell lymphoproliferations display an infrequent association with a latent EBV infection and that the pathogenic role of the virus in the positive cases remains obscure as the virus frequently infects only a minority of the atypical cells.
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PMID:Low incidence of Epstein-Barr virus presence in primary cutaneous T-cell lymphoproliferations. 874 41

A cohort of rhesus macaques (Macaca mulatta), obtained from the California Regional Primate Research Center (CRPRC) and necropsied in 1970-72 with lesions suggestive of simian immunodeficiency virus (SIV) infection, was identified at the New England Regional Primate Research Center (NERPRC). Polymerase chain reaction (PCR), DNA sequence analysis, and in situ hybridization were used to confirm the presence of SIV nucleic acids. This represents the earliest case of SIV infection at the NERPRC and suggests a common source for present day SIV isolates.
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PMID:Origins of simian immunodeficiency virus infection in macaques at the New England Regional Primate Research Center. 875 Oct 50

Chimpanzees infected with human immunodeficiency virus type 1 (HIV-1) are used to model acquired immunodeficiency syndrome (AIDS). Since the central nervous system (CNS) is involved in AIDS, we performed an immunovirological study in 18 chimpanzees inoculated up to 87 months prior to the study (mean, 45 months) with HIV-1 and 8 uninfected controls. Serum and cerebrospinal fluid (CSF) IgG and albumin levels of infected chimpanzees never exceeded those of controls. The CSF/serum albumin ratio was elevated in 1 of 18 infected chimpanzees compared to controls; however, all animals had an elevated ratio indicating a more open blood-brain barrier relative to humans. The intrathecal IgG production index was elevated in only 1 of 18 infected chimpanzees compared to controls. Identical serum and CSF IgG bands were found by isoelectric focusing in 2 of 8 controls and in 1 of 18 infected chimpanzees. None of these bands reacted with recombinant HIV-1 p24gag or gp 120env. HIV-1 was isolated from the peripheral blood of 4 of 18 infected chimpanzees but never from the paired CSF samples. Anti-HIV-1 antibody was detected by a enzyme-linked immunosorbent assay in 18 of 18 paired serum and CSF samples and by Western blot in 18 of 18 serum and 13 of 18 CSF samples from infected chimpanzees without a difference in pattern. Polymerase chain reaction analysis on brain tissue of one animal was negative for HIV-1 sequences. Our results demonstrate that, unlike human infection, chimpanzees inoculated with HIV-1 show no evidence of isolatable virus in the CSF and no evidence of intrathecal anti-HIV-1 antibody synthesis up to several years after experimental infection. The lack of CNS involvement may contribute to the delay or suppression of clinical disease in infected chimpanzees.
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PMID:An immunovirological study of central nervous system involvement during HIV-1 infection of chimpanzees. 879 80

Polymerase chain reaction (PCR) was used for the detection of microsporidian DNA in duodenal biopsies obtained from 28 human immunodeficiency virus (HIV)-infected patients with intestinal microsporidiosis. Duodenal biopsies from 23 HIV-infected patients without microsporidiosis served as controls. A generic primer set for human microsporidia was used at first for the PCR. Amplified products were detected in 26 (93%) of 28 biopsies from patients with intestinal microsporidiosis. All control biopsies were negative. Microsporidia species were identified using Southern blot hybridization with specific probes for Enterocytozoon bieneusi and Encephalitozoon intestinalis. This technique confirmed the transmission electron microscopy-based species identification. Similar results were obtained using PCR with species-specific primer sets for E. bieneusi and E. intestinalis. PCR testing of intestinal biopsy specimens can be used successfully for rapid detection and species differentiation of intestinal microsporidia and thus could be a valuable alternative to transmission electron microscopy.
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PMID:Detection and species identification of intestinal microsporidia by polymerase chain reaction in duodenal biopsies from human immunodeficiency virus-infected patients. 884 34

One hundred fifty-three blood samples from patients positive for the human immunodeficiency virus (HIV) were analyzed by polymerase chain reaction (PCR) to detect the presence of Mycobacterium avium. Samples were collected from patients who also had blood cultures performed by a radiometric method. Blood samples were centrifuged on a Ficoll-Hypaque gradient to purify peripheral blood mononuclear cells. The purified cells were washed and incubated with a resin, boiled to release mycobacterial DNA, and then amplified. Polymerase chain reaction products were detected by a nonisotopic method. A 123 base-pair (bp) insertion sequence, namely IS6110, from Mycobacterium tuberculosis complex was also included in the reaction as an internal control of Taq polymerase activity to exclude the presence of enzyme inhibitors. This IS6110 fragment can be distinguished from the 383 bp target product on ethidium bromide-stained agarose gel and may also be used in a colorimetric assay. Such results were compared with the results of culture and indicated that the assay is as sensitive as bacteriological methods, though faster.
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PMID:Detection and identification of Mycobacterium avium in the blood of AIDS patients by the polymerase chain reaction. 887 71

Polymerase chain reaction (PCR) technology was used to detect Toxoplasma gondii DNA in 253 immunodeficient subjects, 179 of whom were infected with the human immunodeficiency virus (HIV). The incidence of toxoplasmosis was 12.3% (22/179) in the HIV-infected subjects and 2.7% (2/74) in the remainder. The sensitivity of the PCR during episodes of toxoplasmosis in HIV-infected subjects not on antiparasitic treatment was 86.6% on peripheral blood and 60% on cerebrospinal fluid (CSF), but was only 25% and 16.7%, respectively, in subjects receiving specific treatment or prophylaxis against Pneumocystis carinii. Among the HIV-seronegative population, six patients undergoing anticancer chemotherapy were PCR positive on bronchoalveolar lavage fluid but did not develop pulmonary toxoplasmosis, suggesting transient carriage.
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PMID:Detection of Toxoplasma gondii in immunodeficient subjects by gene amplification: influence of therapeutics. 889 3

Human immunodeficiency virus infection of a human bone derived cell line was initiated by either cell free virus or with a cell to cell transmission method. The human bone derived cells were examined for 8 weeks, and virus infection was not detected when assessed by microscopy, immunofluorescence, reverse transcriptase activity, or infection of cocultivated human T lymphoid cells susceptible to human immunodeficiency virus. Polymerase chain reaction analysis of human bone derived cells inoculated with the cell to cell infection format showed less than 0.1% infected cells. It is possible that the infected cells detected by polymerase chain reaction were lymphocytes used in the cell to cell infection format. Alternatively, latent infection may have been established in the bone derived cells with no apparent expression of the proviral genome. A large proportion of bone is represented by human bone derived cells, and it is unlikely that bone will contribute to a significant human immunodeficiency virus reservoir in vivo. The blood of bone allograft donors is likely to have a greater virus bioburden than is bone. Methods to sterilize bone should be assessed by their efficacy to inactivate the virus in blood contaminating the graft, and methods to detect human immunodeficiency virus deoxyribonucleic acid in a bone graft may be less sensitive than examining the donor's blood.
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PMID:Human immunodeficiency virus infection of human bone derived cells. 889 52

CD1a+ dendritic cells (DC) differentiate from a major population of nonadherent CD13(hi)lin- cells that appear when human cord blood CD34+ hematopoietic progenitor cells are cultured with stem-cell factor, granulocyte/macrophage (MA) colony-stimulating factor, and tumor necrosis factor-alpha (TNF-alpha) for 5 days. CD13hilin- cells, which also comprise MA and granulocyte precursors, are CD4+ and can thus be targets of human immunodeficiency virus (HIV). Low replication was noted when these day 5 cells were infected with lymphotropic HIV-1LA1 (p24: < or = 4 ng/mL on day 8 postinfection [PI]), while high virus production occurred with MA-tropic HIV-1Ba-L, HIV-1Ada, or HIV-1-m-n. (p24: 50 to > or = 1,000 ng/mL). Strong cytopathicity (CPE) was then observed in nonadherent cells as in adherent MA. However, FACS analysis on day 7 PI showed that HIV did not affect differentiation of DC that survived CPE: apart from CD4 downmodulation related to HIV production, overall expression of CD40, CD80, and CD86 costimulatory molecules, and of HLA-DR, was unchanged relative to controls. At that time, the capacity of DC from HIV-infected cultures to stimulate the mixed leukocyte reaction was only altered less than 10-fold. Immunocytochemistry on day 7 PI showed that most HIV-infected cells were included in syncytia that were stained by anti-CD1a, anti-S100, and anti-CD14 antibodies, indicating that syncytia consisted of DC and cells of the MA lineage. Polymerase chain reaction analysis of FACS-sorted CD1a+ cells confirmed that they harbored then HIV DNA. Viral DNA was also detected in CD1a+ DC from noninfected cultures that had been exposed to HIV only after sorting. Therefore, we examined whether in infected cultures DC precursors were infected at the onset or if virus spread later from other infected cells to differentiated DC. This was answered by showing that, 24 hours postexposure to HIV, viral DNA was preferentially detected in day 5 sorted CD13hilin- versus CD13hilin- cells, and that it was found in the CD1a+ progeny of CD13(hi)lin- cells 48 hours later. In addition, HIV replication did not affect myeloid clonogenic progenitors in day 0 to day 7 PI cultures, although viral DNA was detected in colony-forming unit-granulocyte/macrophage (CFU-GM)/CFU-M colonies derived from day 3 and 7 PI cultures. Thus, precursors of DC and their progeny are susceptible to HIV in vitro, but, apart from CPE, the effect of virus production on DC differentiation or function is limited.
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PMID:The effect of in vitro human immunodeficiency virus infection on dendritic-cell differentiation and function. 894 57

We have measured the efficiencies of utilization of 8-oxo-dGTP and 8-NH2-dGTP by human immunodeficiency virus type 1 and murine leukemia virus reverse transcriptases and compared them to those of DNA polymerases alpha and beta. Initially, we carried out primer extension reactions in the presence of dGTP or a dGTP analog and the remaining three dNTPs using synthetic DNA and RNA templates. These assays revealed that, in general, 8-NH2-dGTP is incorporated and extended more efficiently than 8-oxo-dGTP by all enzymes tested. Second, we determined rate constants for the incorporation of each analog opposite a template cytidine residue using steady state single nucleotide extension kinetics. Our results demonstrated the following. 1) Both reverse transcriptases incorporate the nucleotide analogs; discrimination against their incorporation is a function primarily of Km or Vmax depending on the analog and the enzyme. 2) Discrimination against the analogs is more stringent with the DNA template than with a homologous RNA template. 3) Polymerase alpha exhibits a mixed kinetic phenotype, with a large discrimination against 8-oxo-dGTP but a comparatively higher preference for 8-NH2-dGTP. 4) Polymerase beta incorporates both analogs efficiently; there is no discrimination with respect to Km and a significantly lower discrimination with respect to Vmax when compared with the other polymerases.
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PMID:Incorporation of the guanosine triphosphate analogs 8-oxo-dGTP and 8-NH2-dGTP by reverse transcriptases and mammalian DNA polymerases. 903 7

Pharyngeal colonization by Streptococcus pneumoniae was evaluated in 103 human immunodeficiency virus (HIV)-infected subjects (<200 CD4 cells/microL, 57; > or = 200 CD4 cells/microL, 46) and 39 non-HIV-infected controls who were participants in a vaccine study. At baseline, 7%, 20%, and 10% of subjects in the <200 and > or = 200 CD4 cell groups and in the control group were colonized with S. pneumoniae: Rates at 6 months were 23%, 22%, and 0%, respectively. Of 34 isolates from HIV-infected subjects, 25 were penicillin-resistant and 19 were resistant to > or = 3 antimicrobials; of 8 isolates from controls, 1 was resistant. Resistance to trimethoprim-sulfamethoxazole was significantly higher among HIV-infected subjects with <200 CD4 cells/microL than in those with more CD4 cells. Polymerase chain reaction DNA analysis with BOX primers demonstrated that 12 HIV-infected subjects were persistently colonized with the same S. pneumoniae strain for > or = 1 month compared with none of the controls. HIV-infected subjects were more likely to be persistent pneumococcal carriers and to carry antibiotic-resistant isolates than were non-HIV-infected subjects.
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PMID:Colonization by Streptococcus pneumoniae among human immunodeficiency virus-infected adults: prevalence of antibiotic resistance, impact of immunization, and characterization by polymerase chain reaction with BOX primers of isolates from persistent S. pneumoniae carriers. 904 30


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