Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Out of a total of 1,600 foreign students who came to India between June 1989 and October 1990, 22 were seropositive for HIV-1. Ten showed antibodies to all the gene products. Antibodies to gp160 and p24 were present in all the seropositives while antibodies to p53, p15/17 were significantly higher in healthy seropositives than in patients with full blown AIDS. Absence of antibodies to p15/17 and p53 thus appeared to be a more sensitive criterion of end stage disease than absence of anti- p24 antibodies. When seropositive samples from African students were checked for HIV-2 antibodies by ELISA, 13/22 were found to be positive. Further, 2/10 Indians with full blown AIDS were also strongly positive for HIV-2. These data could be of relevance for formulating future strategies for population-based screening for HIV-2.
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PMID:Comparative evaluation of HIV infected foreign students and Indian with AIDS in Chandigarh, India. 130 16

A monoclonal antibody-based antigen capture enzyme-linked immunosorbent assay (ELISA) was developed and employed to detect p24 capsid antigen from human T-cell lymphotropic viruses type I and II (HTLV-I, HTLV-II), simian T-cell lymphotropic virus type I (STLV-I)-infected cell lines, and from mononuclear cell cocultures of HTLV-infected humans and STLV-I infected monkeys. A monoclonal antibody specific for HTLV p24 and p53 capsid antigens was coated onto 96-well microtiter plates to capture HTLV/STLV antigen. Captured antigen was then detected by the addition of a polyclonal, biotinylated human anti-HTLV-I antibody, and color developed with tetramethyl benzidine/H2O2 substrate. As little as 15 pg/ml of HTLV-I p24 antigen could be detected in this assay. Culture supernatants from HTLV-I-infected cell lines (HUT-102, MT-2, C5/MJ, HTLV-II-infected cell lines (Mo-T, Mo-B, PanG 12.1, NRA) and STLV-I-infected cell lines (Matsu, NEPC M39) were all positive in the assay. In addition, p24 was detected from peripheral blood mononuclear cell (PBMC) cocultures of 8 of 8 (100%) HTLV-I diseased patients, 14 of 20 (70%) HTLV-I and HTLV-II-infected, asymptomatic persons, and 8 of 8 (100%) STLV-I-infected, asymptomatic monkeys. Culture supernatants of cells infected with human immunodeficiency virus type (HIV-1), simian immunodeficiency virus (SIV), Chlamydia trachomatis, cytomegalovirus (CMV), herpes simplex I and II (HSV), feline leukemia virus (FELV), bovine leukemia virus (BLV), and bovine immunodeficiency virus (BIV) were all negative. Similarly, normal human peripheral blood mononuclear cells and uninfected, transformed human T cells, were also negative in the assay.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of a monoclonal antibody-based p24 capsid antigen detection assay for HTLV-I, HTLV-II, and STLV-I infection. 131 63

The data presented here indicate that the pathogenesis of AIDS-NHL is variably associated with multiple genetic alterations including monoclonal EBV infection, oncogene activation (c-myc, N-, Ki-ras) and tumor suppressor gene (p53) inactivation. Up to three (3 cases) or four (1 case) different lesions have been observed in the same tumor. The distribution of these lesions among the various histotypes is heterogeneous, although some preferential associations have been found either between lesion and histotype or between lesions. The most notable case involves p53 mutations/loss that is exclusively associated with the SNCC lymphoma subtype. Since alterations of the c-myc gene occur at very high frequency in this same histotype it is possible that both lesions may be required for the pathogenesis of the BL phenotype. The consistent negativity of p53 lesions in other NHLs associated or non associated with HIV infection (18) reinforces this hypothesis. Finally, we note that the frequency of p53 mutations is significantly higher in AIDS-BL than in non HIV-related BL (18), although the significancy of this difference remains to be assessed. This study confirms the relatively low frequency of EBV infection in systemic AIDS-NHL in general, but reinforces the notion that EBV may be required for the pathogenesis of AIDS-LC-IBP, as recently suggested by the high frequency of EBV positivity in primary CNS AIDS-NHL which are mostly represented by LC-IBP (2). Conversely, the low frequency of EBV sequences in the AIDS-SNCC lymphomas appears similar to that observed in sBL. Only in a small minority of cases were ras oncogene mutations found, mostly associated with the BL type.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular pathogenesis of HIV-associated lymphomas. 132 69

A total of 40 multiple sclerosis (MS) patients from Denmark and 10 from the Faroes were examined for antibodies with affinity to human T cell leukemia/lymphoma virus type 1 (HTLV-I) and human immunodeficiency virus type 1 and 2 (HIV-1 and HIV-2). Using ELISA, MS patients and a group of healthy controls did not differ significantly in their reactivities to HTLV-I. However, elevated reactivities were recorded with 5 MS sera, whereas only 2 of the sera from the controls produced highly values. Ten patients with other neurological diseases all seemed to exhibit low reactivity in HTLV-I ELISA. The reactivities of 2 MS sera decreased considerably by absorption with an HTLV-I lysate. In immunofluorescence assay, two other MS sera reacted with HTLV-I transformed cell lines as well as with non-infected cells. Examined by Western blotting (WB), a single MS serum produced a distinct HTLV-I p19 band. With ELISA for detection of HIV-1 and HIV-2 antibodies, 2 MS sera exhibited borderline reactions. Further examination of these two sera by WB revealed weak reactivities against p24 and p53 of HIV-1. One the whole, the present observations do not suggest that a putative MS retrovirus would be closely related with HTLV-I, HIV-1 or HIV-2.
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PMID:Seroreactivity to human T cell leukemia/lymphoma virus type 1 and related retroviruses in multiple sclerosis patients from Denmark and the Faroes. 132 31

Chronically immunosuppressed individuals are susceptible to lymphoreticular tumors. Up to 15% of patients with congenital deficiencies such as ataxia=telangiectasia may develop malignancies, mainly high-grade B cell non=Hodgkin's lymphomas (NHLs). AIDS lymphomas are comprised of NHLs including Burkitt's lymphoma (BL) and primary cerebral lymphomas (PCLs). Almost 3% of all AIDS patients (2824 of 97,258 cases) developed NHL. Epstein-Barr virus (EBV) as a co-factor in AIDS lymphomagenesis has been studied: in 12 cases of 24 AIDS lymphomas EBV by DNA in situ hybridization was found. In an analysis of 6 primary cerebral lymphomas, .5 were positive for EBV DNA by Southern blotting. In Burkitt's lymphoma the characteristic genetic alteration affects the c-myc oncogene. In 1/3 of BL p53 mutations were found but none in the 43 NHLs suggesting that p53 mutations and c-myc activation act synergistically in the pathogenesis of these tumors. Cytotoxic agents dideoxyinosine, dideoxycytosine, and zidovudine may cause secondary neoplasia. 8 of 55 AIDS patients under zidovudine treatment developed high-grade lymphoma 23.8 months subsequently; recently doses were reduced. PCL was found in 21 of 90 patients. A 5.2 months survival was associated with combined treatment with cyclophosphamide, Oncovin (vincristine), methotrexate, etoposide, and cytosine arabinoside compared with 11.3 months with chemotherapy. Colony-stimulating factors (CSFs) alleviate drug-induced myelotoxicity and zidovudine-induced neutropenia, however, l8 of 11 patients receiving granulocyte-macrophage CSF developed hematological toxicity. Interleukine-2 produced by T-helper cells enhancing tumor cells cytotoxicity has been used in AIDS-associated cryptosporidial diarrhea and in 4 patients with AIDS lymphoma with modest response, but its stimulation of the HIV-infected substrate may increase viral proliferation.
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PMID:AIDS lymphomas. 161 63

We analyzed sera collected during 1987 and 1988 from 385 healthy business employees of both sexes, of Ogun state in Nigeria, for antibodies to the 3 human retroviruses HIV-1, HIV-2 and HTLV-I. No serum was HIV-1 positive, 1 was HIV-2 positive and 2 were HTLV-I positive. A few sera were false-positive in the antibody screening tests which preceded the confirmatory antibody tests. In the confirmatory tests, we found that in the HIV-1 Western blot test 1 serum reacted only with the HIV-1 gag protein p17, and 2 sera reacted only with the HIV-1 pol proteins p64, p53 and p31. None of these reactivities fulfill internationally accepted criteria for HIV-1 seropositivity. We conclude that HIV-1 was rare in the study population and that HIV-2 and HTLV-I are present at a low frequency. The false positive serological reactions observed are similar to those described previously from Africa and elsewhere. The findings emphasize the importance of routinely testing blood donations for antibodies to these retroviruses in Nigeria.
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PMID:Seroepidemiology of human retroviruses in Ogun State of Nigeria. 197 90

We have performed a prospective 33-month follow-up of the evolution of HIV infection in a cohort of 76 HIV-positive intravenous drug users (IVDUs). We report on immunological and serological variables that proved to be highly predictive of development to AIDS. In a stepwise multivariate analysis of the actuarial progression rate we found the number of CD4+ lymphocytes to be the most powerful predictor of progression to AIDS. We found no independent predictive effects associated with any other variable with predictive power: loss of antibody to p24 antigen, anergy, HIV p24 antigenaemia, loss of antibody to p53 (reverse transcriptase), decreased number of CD8+ T cells, loss of antibody to p31, loss of antibody to p17, beta 2-microglobulin level, loss of antibodies to gp41 and p64, or immunoglobulin A level. We have found that our data differ from those obtained in studies in homosexual men in the different prognostic value of those predictive markers. Our findings should help to identify high risk of progression to clinical AIDS among IVDUs, thereby assisting in the selection of patients for prophylaxis and therapy.
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PMID:Immunological and serological markers predictive of progression to AIDS in a cohort of HIV-infected drug users. 197 43

A 25-year-old Chinese woman, was found HIV antibody positive on December 14, 1988. During our follow-up, we tested her American husband and found him to be seronegative. Unfortunately, her six-month-old infant was seropositive. The standard Western blot test was used in the first stage of analysis. The bands which appeared on the infant's strip were p15, p24, p31, p55 and gp120/gp160, but using the modified Western blot test the bands which appeared were p15, p24, p31, gp41, p53, p55, p64 and gp120/gp160. All the bands appearing on the infant's strips which used a modified Western blot test had higher intensities than those of a standard procedure. The mother was apparently infected with HIV through intercourse with her ex-boyfriend, who was a European. AZT was given to the mother because her T4 cell count was 338 per microliter and because of persistent cervical lymphadenopathy. The infant, which was bottle-fed and had been delivered by caesarean section, may have become HIV infected during the uterine stage.
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PMID:Taiwan's first case of perinatal transmission of HIV confirmed by a modified western blot test. 221 74

A fragment of HTLV-IIIB gag-gene, coding for the first 441 amino acids of the p53 gag-precursor was expressed in the recombinant vaccinia virus, vC5. Two HIV specific proteins were detected by western blot in CV-1 cells infected with vC5. Their relative molecular masses were 50 and 35 Kd, pointing out that the first of the proteins is a full length expression product of the cloned sequence, while the second one is a result of processing or abortive translation. Possibilities of using such a strain as a vaccine or in Western blot conformation test are discussed.
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PMID:[Expression of gag gene of human immunodeficiency virus in recombinant vaccinia virus]. 326 87

Sera from hemophiliacs were analyzed for antibodies to human immunodeficiency virus type 1 (HIV-1) by using radioimmunoprecipitation (RIP), western blotting (WB) with nonreducing buffer (NR), and WB with reducing buffer (R). We analyzed envelope gp160, gp120, and gp41; pol gene proteins p64, p53, and p34; and gag gene protein p24. Of 215 samples positive for reactivity to gp160 and gp120(RIP), antibodies to p24 were undetectable in 2 (0.9%), to gp41 in 9 (4.2%), to the pol antigens in 5 (2.3%), to gp120(NR) in 3 (1.4%), and to gp120(R) in 55 (25.6%). By sequential analysis of samples, antibodies to gp120(NR), gp120(R), p24, gp41, p64/53, and p34 were observed later in the course of infection than were antibodies to gp120(RIP) or gp160. This result suggests caution against reliance on WB as the "gold standard." A significantly higher rate of progression to AIDS-related complex was found for individuals lacking antibodies to gp120(R). It is possible that antigenic domains represented by gp120(R) may play a role in the pathogenesis of HIV-1 infection.
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PMID:Antibody responses in early human immunodeficiency virus type 1 infection in hemophiliacs. 334 72


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