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)

Kaposi's sarcoma (KS) is a neoplasm of multifocal origin which manifests primarily as multiple vascular nodules in the skin and other organs. Its association with HIV has been reported in America, Africa, and Europe. Extremely rare in HIV-infected women and children, the condition is reported more commonly in homosexual males. It is suspected that female hormones may protect women against KS. The first case of AIDS-associated KS in a 35-year old Indian female prostitute is reported for its rarity and clinico-epidemiological implications in the Indian setting. The woman presented with multiple painless non-pruritic nodules of varying colors on the right leg with swelling since two months. There was no history of trauma, discharge from the lesions or any treatment taken, nor any history of blood transfusion, IV drug use, or sexually transmitted disease. On examination, present mainly on the right leg were multiple, nontender papulonodules, reddish to purplish in color, 2-10 mm in diameter, and adherent to skin and underlying structures but not to the bone. Few discrete similar lesions were seen on the right forearm and left side of chin and left leg. Telangiectasia was noted on the anteromedial part of the right knee and ears and molluscum contagiosa on the front of the chest, while bilateral non-pitting oedema was apparent up to the knee. Inguinal and supraclavicular lymph glands were palpable. A raised purplish plaque was seen on the hard palate and in front of the left upper lateral incisor on the gingiva with candidiasis of the dorsum of the tongue, and there was congestion of the right lower palpebral conjunctiva, while a systemic examination proved normal. The diagnosis of KS was confirmed by histopathology, electron microscopy, seropositivity, and Pepti-LAV test and viral culture. Antibodies were found to HIV-1 and HIV-2, and HLA DR5,7 was positive on oligotyping. On treatment, initially, very few skin lesions flattened almost totally after intralesional injection of vincrysticine. Alpha interferon 200 IU sublingually daily showed amelioration in palatal, gingival, chin, forearm, and right leg lesions within a fortnight. The patient is receiving tab ketoconazole orally, 200 mg bid for oral and esophageal candidiasis and tab cimetidine as an immunomodulator. Since cutaneous lesions of KS are radiosensitive, local radiotherapy for leg lesions is contemplated.
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PMID:AIDS-associated Kaposi's sarcoma in an Indian female. 827 May 82

Photochemical decontamination (PCD) of platelet concentrates, with adequate preservation of platelet function, has been shown using 8-methoxypsoralen (8-MOP) and long wavelength UV light (UVA). To further evaluate this technique, models for the inactivation of pathogenic human cell-associated viruses and integrated proviral sequences are required. We have assessed the ability of the PCD technique to inactivate cell-associated human immunodeficiency virus 1 (HIV-1) in platelet concentrates. We correlated PCD inhibition of HIV-1 infectivity with 8-MOP-DNA adduct formation in contaminating nucleated cells, and measured the inhibition of polymerase chain reaction (PCR)-mediated amplification of cellular DNA sequences as a surrogate for inactivation of integrated proviral nucleic acid sequences. After PCD treatment (8-MOP 300 micrograms/mL, UVA 17 mW/cm2) for 60 minutes, 0.5 x 10(6) plaque-forming units (PFU)/mL of cell-associated HIV-1 were inactivated and no virus was detectable by infectivity assay. After 60 minutes of PCD, 15 8-MOP-DNA adducts per 1,000 bp were formed, while in the absence of UVA, no adducts were formed. PCR-mediated amplification of a 242-bp cellular DNA sequence (HLA-DQ-alpha) was inhibited when greater than eight psoralen-DNA adducts per 1,000 bp were present. These studies indicate that high titers of cell-associated HIV-1 in platelet concentrates were inactivated by PCD, and the numbers of 8-MOP-DNA adducts in nucleated cells were sufficient to inhibit amplification of DNA segments that encode for as few as 80 amino acids. Based on the frequency of 8-MOP-DNA adducts, for the 10-kb HIV-1 genome, the probability of an integrated genome without at least one 8-MOP adduct after 60 minutes of PCD was 10(-33).
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PMID:Photochemical inactivation of cell-associated human immunodeficiency virus in platelet concentrates. 832 30

This study examines plaque for the presence of a recently described oral spirochete, tentatively called pathogen-related oral spirochete. This investigation found PROS in plaque of patients with HIV-associated periodontal disease.
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PMID:HIV-associated periodontal disease: new oral spirochete found. 833 2

Data from cross-sectional studies suggest that periodontitis in HIV-infected patients is a more destructive form of disease in contrast to the slowly progressing form of adult periodontitis in the general population. We studied prospectively over an 18-month period 30 HIV infected, but asymptomatic, patients and compared the rate of periodontal attachment loss with that of a healthy control group (n = 10) matched for age and plaque index. Every 6 months, each subject was assessed for their clinical status by a physician and CD4+ cell count determined. The proliferative response of peripheral blood lymphocytes was determined by in vitro cultures with PHA and Con A. The periodontal health status was assessed by scoring with plaque index (PI), gingival index (GI), and periodontal disease index (PDI). The control subjects were assessed for periodontal status only. Of the 30 HIV-positive patients whose data were analyzed 14 received Zidovudine (AZT) while the remaining 16 did not. There was no correlation between any clinical parameter measured and periodontal status as determined by PI or GI. However, a significant difference in the change of periodontal disease index (PDI) was observed between the HIV-infected and control groups (P = 0.005). We concluded that HIV-infected patients with pre-existing periodontitis tend to experience a greater rate of attachment loss over time compared with controls.
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PMID:Progression of periodontal disease in HIV seropositive patients. 836 14

Human immunodeficiency virus (HIV-1) is generally transmitted by parenteral contact with infected body secretions. Although extensive epidemiological data and familial studies have failed to provide any conclusive data that saliva may act as a vehicle for transmission of AIDS, both professional and public anxieties remain. The present study, as well as others, suggests that salivary secretions may act as inhibitors of HIV-1 replication in vitro. In our study, the inhibitory activity was determined to be associated mainly with secretions obtained from the human submandibular-sublingual glands. Human submandibular-sublingual (HSMSL) and parotid (HPS) salivas were collected and tested for their ability to modulate the replication of HIV-1, using a plaque assay on HeLa/CD4+ cell monolayers. Initial results examining freshly collected salivary samples from ten individuals confirmed the results previously obtained by Fox et al. (1988, 1989). An average plaque reduction of approximately 66% was obtained with HSMSL, in contrast to 34% reduction obtained with HPS. Titration of the inhibitory activity in HSMSL showed detectable levels at a 1:500 dilution. Comparison of inhibitory activity of dialyzed and lyophilized saliva to fresh saliva indicated little difference between the two samples when filtration occurred after the addition of HIV-1. However, the effect of filtration was significantly diminished in the lyophilized samples. Electron microscopic examination of the saliva-HIV incubates revealed the aggregation/entrapment of virus particles by salivary components. These results suggest that human salivary secretions (with HSMSL > HPS) may have a role in modulating the infectivity of HIV-1.
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PMID:Aggregation of human immunodeficiency virus type 1 by human salivary secretions. 837 99

Rationally designed synthetic inhibitors of retroviral proteases inhibit the processing of viral polyproteins in cultures of human immunodeficiency virus type 1 (HIV-1)-infected T lymphocytes and, as a result, inhibit the infectivity of HIV-1 for such cultures. The ability of HIV-1 protease inhibitors to suppress replication of the C-type retrovirus Rauscher murine leukemia virus (R-MuLV) and the HIV-related lentivirus simian immunodeficiency virus (SIV) was examined in plaque reduction assays and syncytium reduction assays, respectively. Three of seven compounds examined blocked production of infectious R-MuLV, with 50% inhibitory concentrations of < or = 1 microM. Little or no cellular cytotoxicity was detectable at concentrations up to 100 microM. The same compounds which inhibited the infectivity of HIV-1 also produced activity against SIV and R-MuLV. Electron microscopic examination revealed the presence of many virions with atypical morphologies in cultures treated with the active compounds. Morphometric analysis demonstrated that the active compounds reduced the number of membrane-associated virus particles. These results demonstrate that synthetic peptide analog inhibitors of retroviral proteases significantly inhibit proteolytic processing of the gag polyproteins of R-MuLV and SIV and inhibit the replication of these retroviruses. These results are similar to those for inhibition of HIV-1 infectivity by these compounds, and thus, R-MuLV and SIV might be suitable models for the in vivo evaluation of the antiretroviral activities of these protease inhibitors.
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PMID:Antiretroviral activities of protease inhibitors against murine leukemia virus and simian immunodeficiency virus in tissue culture. 838 40

To study the role of IL-6 in HIV-induced B cell defects, in vitro B cell responses and IL-6 secretion were determined simultaneously in 67 haemophilia patients. Twenty-three patients were HIV- (Group 1), 27 HIV+ stage CDC II, III (Group 2), and 17 were HIV+ stage CDC IV (Group 3). Pokeweed mitogen (PWM) was used for T cell-dependent and Staphylococcus aureus Cowan I (SAC I) for T cell-independent B cell stimulation. B cell differentiation was assessed in a reverse haemolytic plaque assay and by ELISA determination of IgG and IgM in culture supernatants. An ELISA was used to measure IL-6 in plasma and culture supernatants. HIV- patients showed impaired immunoglobulin-secreting cell (ISC) responses after T cell-independent and T cell-dependent stimulation (P < 0.0001 and P < 0.01, respectively), whereas IL-6 secretion, IgM and IgG responses were comparable to those in healthy controls. HIV+ patients at stage CDC II, III or IV demonstrated significantly reduced mitogen-stimulated IL-6 secretion (P < 0.05, PWM; P < or = 0.001, SAC I) as well as impaired ISC and IgG responses (P < 0.01, PWM; P < or = 0.0001, SAC I). CDC IV patients showed reduced IgM responses in addition (P < 0.02, PWM; P < 0.0005, SAC I). Plasma IL-6 levels were elevated both in HIV+ patients (CDC II, III patients: 165 +/- 73 pg/ml, P < 0.005; CDC IV patients: 58 +/- 18 pg/ml, P < 0.0001) and in HIV- patients (283 +/- 65 pg/ml, P < 0.0001) which appeared to be a T cell effect induced by treatment with haemophilia factor concentrates. Our data provide evidence for different types of B cell deficiencies in HIV- patients (impaired ISC response only) and HIV+ patients (impaired ISC as well as IL-6 and IgM/IgG responses). The defective IL-6 secretion in HIV+ patients is likely to affect terminal B cell differentiation and this may explain the reduced immunoglobulin secretion in these patients in response to antigenic challenge.
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PMID:Defective IL-6 secretion in HIV-infected haemophilia patients. 842 91

A simple, sensitive and accurate plaque assay was developed using HPB-Ma, a variant of the human T-cell line HPB-ALL, which becomes adherent to the substratum after infection with an amphotropic murine sarcoma virus (MSVa). The simplicity of this novel plaque assay allowed us to examine a large number of serum samples from patients with HIV infection for neutralizing antibody activity against two human immunodeficiency virus type-1 (HIV-1) strains. During the progression of clinical disease, the neutralizing activity in the sera from two individual patients remained unchanged or increased. A patient with a known time of HIV infection produced cross-neutralizing antibody at 25-34 weeks. The neutralizing activity in the sera from 17 asymptomatic carriers, four patients with AIDS-related complex and four AIDS patients was also examined and was found to be unrelated to the clinical stage.
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PMID:New HIV plaque titration; application to the assay of neutralizing antibody. 843 63

From January 1988 to December 1993, we identified six men with minimally invasive (stage I) squamous cell carcinoma of the anus and 10 men with anal carcinoma in situ (CIS). Of the six patients with invasive carcinoma, four were infected with human immunodeficiency virus (HIV), including one with AIDS. Of the 10 patients with CIS, eight were infected with HIV, including four with AIDS. Anal pain and bleeding were the most common symptoms of minimally invasive anal cancer and anal CIS. Anal irritation, burning, or pruritus occurred more frequently in patients with CIS, whereas anal ulcers, masses, or abscesses were more frequent in patients with minimally invasive cancer. Several patients with CIS had a discrete area of leukoplakia in the anal canal or a pigmented plaque of the anus and anal canal. These lesions were not observed in patients with minimally invasive anal cancer. The symptoms and signs of early-stage anal cancer in men at risk for developing HIV infection or men infected with HIV often resemble those of other common anorectal diseases in homosexual men. Anal cancer in HIV-infected men is not limited to those individuals with AIDS.
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PMID:Clinical presentation of minimally invasive and in situ squamous cell carcinoma of the anus in homosexual men. 852 51

The stoichiometry of human immunodeficiency virus type 1 (HIV-1) inactivation by soluble receptor CD4-IgG hybrid dimers (CD4-IgG) was examined. The extent of HIV-1 inactivation was measured in a sensitive plaque-forming assay, and the corresponding level of CD4-IgG binding was determined by immunofluorescence of infected cells. Ninety percent virus inactivation occurred at relatively low levels of CD4-IgG binding (10% of the saturating level). At even lower binding levels (1.4% of maximum binding), virus survival was 44%. Over a broad range of binding conditions, the survival curve followed a model in which viruses binding more than a threshold level of CD4-IgG were completely inactivated, while viruses binding less remained infectious. The data indicate that CD4-IgG binding to 1.4% of gp120 binding sites equals the threshold for inactivation. Thus, virus inactivation can begin when 3 CD4-IgG (of approximately 216 gp120 sites) bind per virion.
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PMID:CD4-IgG binding threshold for inactivation of human immunodeficiency virus type 1. 860 64


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