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)

A patient with pneumococcal septicaemia and serological evidence of infection with human immunodeficiency virus (HIV) presented with a peripheral T-cell lymphoma. As far as we are aware this association has not been reported previously.
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PMID:T-cell lymphoma associated with human immunodeficiency virus (HIV) infection. 207 79

Immunophenotypic analysis on 34 cases of T-cell malignancies using monoclonal antibodies against T-cell receptors (TCR) revealed 25 cases of alpha beta-type and two of gamma delta-type. The two patients with gamma delta-type showed cutaneous involvement of tumor cells. Immunoblastic lymphadenopathy (IBL)-like T-cell lymphoma is divided into three histologic categories; inconspicuous type, patchy type and diffuse type. DNA hybridization analysis revealed that 11 of 16 cases showed clonal rearrangement of TCR beta-chain gene without rearrangement of immunoglobulin heavy chain gene, providing strong evidence for clonal proliferation of T-cells. Among 185 patients with adult T-cell leukemia (ATL), 18 cases (9.7%) were found not to be associated with human T-cell leukemia virus type I (HTLV-I). They consisted of 10 of acute type, five of chronic type, two of lymphoma type and one of smoldering type, indicating a diversity in clinical features. Two Japanese patients with ATL developed secondary monoclonal B-cell lymphomas of diffuse, large cell, non-Burkitt type. They were seropositive for HTLV-I but negative for human immunodeficiency virus (HIV). They also suffered from pulmonary tuberculosis, and one from adenovirus type 11-induced hemorrhagic cystitis, indicating an immunodeficient state. Epstein-Barr virus genome was found in lymphoma cells from one patient. It is suggested that opportunistic B-cell lymphomas may occur in the immunodeficient stage of ATL.
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PMID:[Recent advances in clinical research on T-cell lymphoma]. 239 7

A patient with cutaneous T-cell lymphoma (CTCL) and acquired immune deficiency syndrome (AIDS) is presented. The patient had a localized lesion on his scalp. Evaluation for systemic lymphoma was negative. A biopsy specimen showed superficial and deep dermal infiltrates of pleomorphic lymphocytes. Immunohistochemistry was consistent with T-cell lymphoma. The patient was treated successfully with local irradiation. He remained free of further systemic and cutaneous recurrences of the lymphoma until he died 8 months after treatment of pneumonia. This case is the first to our knowledge to describe a localized CTCL in a patient infected with human immunodeficiency virus type 1 (HIV-1).
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PMID:Cutaneous T-cell lymphoma in a patient infected with human immunodeficiency virus type 1. Use of radiation therapy. 240 Sep 64

The evidence that schizophrenia may involve infection by a virus (or viruses) has been indirect. The recent discovery, however, of the human retroviruses--human T-cell lymphoma-leukemia virus-I, and II (HTLV-I, -II) and human immunodeficiency virus (HIV)--now also known to affect the central nervous system (CNS), together with the development of new techniques in retrovirology, have made it possible to investigate more directly the role of this class of viruses as an etiology of schizophrenia. In our first effort to screen for the presence of a T-cell lymphotropic virus in schizophrenia, short-term tissue cultures of peripheral lymphocytes from 17 chronic schizophrenic patients and 10 normal controls were established. The cells were cultured in the presence of T-cell growth factor (TCGF, IL-2), and the culture supernatants were tested for the presence of the retroviral enzyme reverse transcriptase. No T-cell-associated reverse transcriptase activity was detected in cultures from patients or normal controls. Therefore, the data do not provide evidence for a role for T-cell lymphotropic retroviruses as an etiology of schizophrenia.
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PMID:Lack of evidence for a role of T-cell-associated retroviruses as an etiology of schizophrenia. 246 91

The enzymatic amplification of specific nucleic acid sequences in vitro has revolutionized the use of nucleic acid hybridization assays for viral detection. With this method, the copy number of a pathogen-specific sequence is increased several orders of magnitude before detection is attempted. The sensitivity and specificity of detection are thus markedly improved. Mullis and Faloona devised the first method of sequence amplification in vitro, the polymerase chain reaction (K.B. Mullis and F.A. Faloona, Methods Enzymol. 155:355-350, 1987). By this method, synthetic oligonucleotide primers direct repeated, target-specific, deoxyribonucleic acid-synthetic reactions, resulting in an exponential increase in the amount of the specific target sequence. The application of sequence amplification to viral detection was initially performed with human immunodeficiency virus type 1 and human T-cell lymphoma virus type I. In principle, however, this approach can be applied to the detection of any deoxyribonucleic or ribonucleic acid virus; the only requirement is that sufficient nucleotide sequence data exist to allow the synthesis of target-specific oligonucleotide primers. The use of target amplification in vitro will permit a variety of studies of viral pathogenesis which have not been feasible because of the low copy number of the viral nucleic acids in infected material. This approach is particularly applicable to the study of human retroviral infections, which are chronic and persistent and are characterized by low titers of virus in tissues. In addition, target amplification in vitro will facilitate the development of new methods of sequence detection, which will be useful for rapid viral diagnosis in the clinical laboratory.
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PMID:Nucleic acid amplification in vitro: detection of sequences with low copy numbers and application to diagnosis of human immunodeficiency virus type 1 infection. 265 Aug 62

The majority of lymphomas that develop in human immunodeficiency virus type 1 (HIV-1) positive patients have a B-cell phenotype, with few reported cases of T-cell lymphoma. Within the latter group, those that have been comprehensively phenotyped had a mature helper T-cell phenotype (CD4+). We report, for the first time, an HIV-1 positive patient with a precursor T-cell lymphoma (CD7+,CD1-,CD3-,CD4-, and CD8-). T-cell receptor beta and gamma genes were in the germline configuration and integration of HIV-1 DNA could not be detected in the lymphoma cell genome.
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PMID:Precursor T-cell lymphoma associated with human immunodeficiency virus type 1 (HIV-1) infection. First reported case. 278 49

Immunoblastic lymphadenopathy (IBL)-like T-cell lymphoma is a distinct peripheral T-cell lymphoma, which closely resembles angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) and/or IBL, but is characterized by focal or sheet-like proliferation of immunoblasts and pale cells of T-cell nature. In this report, 36 patients with IBL-like T-cell lymphoma were analyzed. The disease is clinically characterized by generalized lymph node swelling, hepatosplenomegaly, fever, skin rash, polyclonal hypergammaglobulinemia, marked male predominance, predilection for the elderly, and poor prognosis. There was no association with human T-cell leukemia virus type I or human immunodeficiency virus. IBL-like T-cell lymphoma may be divided into two categories (CD4+ type and CD8+ type) by surface marker analysis. It can also be divided into three categories on the basis of the histologic findings of distribution of morphologically recognizable tumor cells: nine cases of "inconspicuous type," six cases of "patchy type," and 21 cases of "diffuse type." Two cases of "inconspicuous type" converted later to "diffuse type." DNA hybridization analyses in the ten recent cases revealed that three of four "inconspicuous types" and five of six "diffuse types" showed clonal rearrangement of T-cell receptor-beta chain gene without rearrangement of immunoglobulin heavy chain gene, providing strong evidence for clonal proliferation of T cells.
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PMID:Clinicopathologic, immunophenotypic, and immunogenotypic analyses of immunoblastic lymphadenopathy-like T-cell lymphoma. 304 80

We have investigated the effect of isobutyl nitrite on murine NK-cell antitumor-directed cytotoxicity. This agent has been suggested as one of the factors underlying immunodeficiency syndrome (AIDS) in man. We demonstrated that two injections, each of 0.25 ml isobutyl nitrite, resulted in significant depression of endogenous splenic and peripheral blood natural killer (NK) cell cytotoxicity against T-cell lymphoma, YAC-1. In addition to endogenous NK cells, activity of pyrimidinol-activated NK cells was also substantially depressed by this agent. The latter observation is of the utmost importance, since it suggests that the attempt to augment NK-cell activity (to promote resistance to infections and malignancies) could fail in patients with AIDS who are isobutyl nitrite users. Isobutyl nitrite was NK-cell-suppressive not only after in vivo administration but, most importantly, also after inhalation. This indicates that isobutyl nitrite, via its NK-cell suppressive effect, could contribute to immunodeficiency in AIDS. Studies on the mechanism of NK-cell depression by isobutyl nitrite demonstrated that the NK-cell tumor-binding properties as well as NK-cell cytotoxic potential were substantially depressed. Mixing experiments failed to reveal any regulation by suppressor cell activities. The results of these studies clearly indicate that isobutyl nitrite is an immunosuppressive agent and that its use should be avoided.
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PMID:Depression of murine natural killer cell cytotoxicity by isobutyl nitrite. 623 10

In order to better understand the genomic diversity and molecular phylogeny of the human retroviruses, the plasmas from 250 Zairean patients collected in 1969 were tested for antibodies to human T-cell lymphoma and human immunodeficiency viruses (HTLV or HIV) using ELISA and confirmatory Western blots and for viral nucleic acids by reverse transcriptase-directed PCR (RT-PCR). Interestingly, none of the patients was confirmed positive for HIV, even though this region is now endemic for HIV-1. However, 74 (30%) and 3 (1%) of the samples were positive for antibodies to HTLV-I and II, respectively. Forty-four of 74 (59%) Western blot-positive Zairean samples were RT-PCR positive for HTLV-I, while 1 of 3 (33%) of HTLV-II-seropositive samples was RT-PCR positive. On the contrary, none of the Western blot-negative or indeterminate samples were RT-PCR positive for either HTLV-I or HTLV-II. We have cloned and sequenced 140 bp of the pol gene flanked by SK110/SK111 from 8 HTLV-I- and 1 HTLV-II-positive archival samples from Zaire. The HTLV-I isolates from Zaire cluster together as a phylogenetic group, diverging from the prototype Japanese HTLV-I (ATK) by a range of 1.4 to 3.6%. Their close homology to some African STLV-I isolates suggests relatively recent interspecies transmission. The Zairean HTLV-II isolate is closely grouped with the HTLV-II substrain of isolates found in Paleo-Amerindians of the New World, making it unlikely that it represents an endemic African strain.
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PMID:Serological and nucleic acid analyses for HIV and HTLV infection on archival human plasma samples from Zaire. 791 21

To determine the frequency and pattern of neurological complications of T-cell lymphoma (TCL), we retrospectively reviewed the medical records of 316 patients with TCL diagnosed between January 1984 and May 1991. Disease entities not included in this study were lymphoblastic lymphoma, primary central nervous system lymphoma, CD30-positive anaplastic large cell lymphoma, and lymphomas secondary to human immunodeficiency virus or human T-cell lymphotropic virus type I. Cases were classified as having direct complications (parenchymal, leptomeningeal, epidural, or peripheral) or indirect complications (paraneoplastic, disease related, or treatment related). Preexisting neurological conditions were excluded. The overall rate of neurological complications was 7.9%. The frequency of neurological complications in peripheral TCL and cutaneous TCL was 17% and 3%, respectively, with at least half of the neurological complications in both conditions due to direct involvement of the nervous system. Direct neurological complications of TCL were primarily due to leptomeningeal and parenchymal involvement. There were no cases of epidural spinal cord disease.
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PMID:Neurological complications of peripheral and cutaneous T-cell lymphomas. 794 94


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