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)

Whether tuberculosis patients received short-course chemotherapy with treatment of isoniazid (INH) and rifampicin (RIF), combined or not with pyrazinamide (PZA) and ethambutol (EMB) or streptomycin (SM), or long term chemotherapy with INH, SM and thiacetazone (Tb1), the rate of sputum culture conversion was similar in HIV-positive and HIV-negative patients. To prevent relapses it was recommended to treat patients for a minimum of 9 months and for at least 6 months after culture conversion, or even to administer INH for life after the end of treatment. However, no difference was observed in the percentage of relapses between HIV-positive and HIV-negative patients. Side-effects were observed in approximately 20% of HIV-positive patients treated with INH + RIF + PZA + EMB (or SM) or with INH + SM + Tb1, Tb1 being responsible for epidermal necrolysis, in some cases fatal. The mean survival of HIV-patients with tuberculosis was from 10 to 18 months after the diagnosis of tuberculosis. Other opportunistic infections could have been the main cause of death. Acquired drug resistance is not a common complication of tuberculosis treatment in HIV-positive patients, but several epidemics of nosocomial transmission of multiple drug-resistant tuberculosis have recently been observed in the USA. Sparfloxacin, a new fluoroquinolone with a long half-life and low MIC (0.25-0.50 mg/l) against Mycobacterium tuberculosis, is a promising drug against tuberculosis.
Tuber Lung Dis 1992 Dec
PMID:Treatment of tuberculosis in HIV infection. 826 Jun 70

Progress in human cell culture research is discussed based primarily on our hematopoietic cell culture studies. The article includes a historical background of Burkitt lymphoma cell lines, discovery of EBV, normal B-lymphoblastoid cell lines with EBV, a variety of leukemia, lymphoma, and myeloma cell lines, clinical and theoretical contributions made by studies of T-cell leukemia cell lines, the discovery and clinical relevance of HTLV, HIV and HBLV, early attempts at adoptive immunotherapy of patients with cancer, and the future of human cell culture research. Despite the fact that current cell culture methods permit maintenance of only limited cell types of both normal and malignant origins, biotechnological advances such as hybridoma and recombinant DNA technologies should continue to provide unlimited research opportunities in all fields.
Hum Cell 1992 Dec
PMID:Historical progress and the future of human cell culture research. 133 5

Penicilliosis marneffei is a rare deep fungal infection. The endemic area especially located in the Southeast of Asia. In the former literatures till 1990, 29 cases were reported, most of them were diagnosed pathologically from autopsy. Since 1989 there were more reports of P. marneffei in the HIV infected individuals and graft recipient, so far as the increased immunocompromised hosts systemic fungi infection would be a crucial problem. In this report, a case of systemic Penicilliosis marneffei according to biopsy and cultural identification was reported. Amphotericin B was administered in a total dose of 873 mg, and got a good response. The pathogenesis, clinical manifestations and diagnosis were reviewed.
Zhonghua Jie He He Hu Xi Za Zhi 1992 Dec
PMID:[Penicilliosis marneffei. Report of a case and review of literatures]. 133 13

There are now sufficient data to conclude that women infected with human immunodeficiency virus (HIV) have an increased risk of human papillomavirus (HPV) infection and preinvasive stages of cervical cancer. This association is not completely due to immunosuppression. It is likely that HPV pathogenesis is altered in HIV-infected women. Preinvasive cervical neoplasia likely occurs more frequently in HIV-infected women because of several factors, including immunosuppression, viral interactions, and alterations in viral pathogenesis. As new treatments prolong the life of HIV-infected individuals, we must continue to be aware of and reactive to an increasing number of opportunistic complications of HIV infection, such as HPV infection and associated diseases.
Infect Agents Dis 1992 Dec
PMID:Human papillomavirus, human immunodeficiency virus, and cervical cancer: newly recognized associations? 134 70

At least two mechanisms have been implicated in regulating poly(A) site use in human immunodeficiency virus type 1 (HIV-1): inhibition of basal signals within 500 nucleotides (nt) of the cap site, leading to specific suppression of the 5' poly(A) site, and stimulation of basal signals by long terminal repeat U3 sequences, leading to specific activation of the 3' poly(A) site. We determined the relative contributions of these mechanisms in a HeLa cell transcription/processing reaction and by transient transfection analysis. In vitro, the efficiency of basal signals is equivalent close to (270 nt) and far from (1,080 nt) the promoter and is stimulated at least 30-fold in both positions by upstream U3 sequences. In vivo, U3 sequences also enhance processing at both positions. There are two additional effects when the poly(A) site is close to the cap site: at least a 15-fold reduction in total RNA levels and a 5-fold decrease in relative levels of RNA processed at the HIV-1 site in constructs containing U3. Both effects are overcome by insertion of upstream splicing signals in an orientation-dependent manner. Splicing appears to influence poly(A)+ RNA levels by two distinct mechanisms: stabilizing nuclear transcripts and directly stimulating 3' end formation. It is proposed that upstream elements play major roles in regulating poly(A) site choice and in controlling the subsequent fate of polyadenylated RNA. The impact of these findings on mechanisms of mRNA biogenesis in the HIV-1 provirus is discussed.
Mol Cell Biol 1992 Dec
PMID:Relative roles of signals upstream of AAUAAA and promoter proximity in regulation of human immunodeficiency virus type 1 mRNA 3' end formation. 136 Jan 44

Human immunodeficiency virus (HIV-1) infection in the human brain leads to characteristic neuropathological changes, which may result indirectly from interactions of the envelope glycoprotein gp120 with neurons and/or glial cells. We therefore investigated the binding of recombinant gp120 (rgp120) to human neural cells and its effect on intracellular signalling. Here we present evidence that rgp120, besides binding to galactocerebroside or galactosyl-sulfatide, specifically binds to a protein receptor of a relative molecular mass of approximately 180,000 Da (180 kDa) present on the CD4-negative glioma cells D-54, but not on Molt4 T lymphocytes. Binding of rgp120 to this receptor rapidly induced a tyrosine-specific protein kinase activity leading to tyrosine phosphorylation of 130- and 115-kDa proteins. The concentration of intracellular calcium was not affected by rgp120 in these cells. Our data suggest a novel signal transducing HIV-1 gp120 receptor on CD4-negative glial cells, which may contribute to the neuropathological changes observed in HIV-1-infected brains.
Virology 1992 Dec
PMID:HIV-1 gp120 receptor on CD4-negative brain cells activates a tyrosine kinase. 136 Jan 81

Ultrastructural studies suggest that cell surface alterations occur early during the course of HIV-1 infection of CD4+T-lymphoblastoid cells. Attachment and penetration of HIV resulted in formation of membrane discontinuities and pores and "ballooning." Distention of the endoplasmic reticulum occurred in some cells within the first hour after HIV infection, and this correlated with the numbers of virions bound at the cell surface. These results suggest that HIV virion components may directly damage the cell membrane.
Virology 1992 Dec
PMID:Membrane alterations linked to early interactions of HIV with the cell surface. 136 Jan 83

Patients with acquired immunodeficiency syndrome frequently suffer peripheral neuropathy. We investigated its prevalence and relationship to clinical stage of human immunodeficiency virus (HIV) infection using quantitative sensory testing and nerve conduction testing. Vibratory threshold was determined in the right great toe and index finger of 179 men seropositive for HIV (28 with acquired immunodeficiency syndrome [AIDS] or AIDS-related complex [ARC], 151 asymptomatic) and 32 HIV-seronegative controls. None had clinical peripheral neuropathy. Abnormal threshold was control mean plus 2.5 SDs. In the toe, 10 (36%) of 28 subjects with AIDS or ARC had abnormal vibratory thresholds, compared with seven (5%) of 151 asymptomatic seropositive subjects and none of 32 controls. A subgroup of 168 seropositive subjects underwent nerve conduction testing. Abnormality rates were similar, but abnormalities of nerve conduction coincided with quantitative sensory testing abnormalities in only half the cases. Mean (+/-SD) vibratory threshold was significantly greater in subjects with AIDS or ARC (3.00 +/- 0.51 vibratory units) than in asymptomatic subjects (1.56 +/- 0.27 vibratory units) and controls (1.63 +/- 0.54 vibratory units). Finger abnormality rates did not differ, although subjects with AIDS or ARC had greater mean vibratory threshold. Subclinical peripheral neuropathy is thus related to stage of HIV infection and is present by quantitative sensory testing in 36% of patients with AIDS or ARC.
Arch Neurol 1992 Dec
PMID:Sensory testing in human immunodeficiency virus type 1-infected men. HIV Neurobehavioral Research Center Group. 136 Feb 2

Antiretroviral therapy with zidovudine is indicated in patients with CD4 cell counts below 500 per mm3 (500 x 10(6) per L). Patients intolerant of zidovudine and those with advanced human immunodeficiency virus infection may benefit from newer antiretroviral agents, such as didanosine (ddl) or zalcitabine (ddC). Prophylactic therapy for Pneumocystis carinii pneumonia is indicated in patients with CD4 cell counts below 200 per mm3 (200 x 10(6) per L), in patients with CD4 cell counts less than 20 percent of the total lymphocytes and in patients with a prior history of P. carinii infection. In addition, prophylaxis is often initiated if thrush is present, even when CD4 cell counts are above 200. Trimethoprim-sulfamethoxazole is the drug of choice for Pneumocystis prophylaxis; aerosolized pentamidine is reserved for patients unable to tolerate trimethoprim-sulfamethoxazole. Oral candidiasis is treated with nystatin suspension, clotrimazole troches, ketoconazole or fluconazole, with fluconazole used for resistant or more invasive infection. Finally, acyclovir is used to treat herpes zoster or herpes simplex virus infection.
Am Fam Physician 1992 Dec
PMID:Update on drug therapy for HIV and related infections in adults. 835 31

Complement and antibody contribute to infection-enhancement and possible expanded cellular tropism of HIV-1 in vitro through a process requiring complement receptors. Until now, however, the ability of HIV-1 to bind complement receptors has not been documented or characterized. We investigated whether antibody and complement permitted HIV-1 to bind to the B lymphocyte receptor, CR2 (CD21), in an effort to learn more about infection-enhancement, and also because CR2 can mediate B cell proliferation and antigen localization in lymphoid organs in other systems. HIV-1 incubated with antibody and fresh human serum as a source of complement bound approximately 10-fold greater to cells expressing CR2 than to HIV-1-permissive cells lacking this receptor. A similar effect was observed using cells which expressed CR2 but no CD4. This binding was minimal in heat-inactivated and C3-deficient sera, and was significantly reduced by the anti-CR2 MoAb, OKB7, but not by the anti-CD4 MoAb, OKT4a. Thus, complement and antibody acted in concert to facilitate the binding of HIV-1 to CR2 independently of CD4. CD4-independent binding of HIV-1 to CR2 was not sufficient to produce infection in Raji-3 cells. Titres of antibodies mediating CR2 binding correlated with antibody titres as measured by immunofluorescence (P < 0.01) and infection-enhancement (P < 0.05) but were discordant with titres of neutralizing antibodies, a result consistent with the utilization of CR2 for enhanced infection of cells. The ability of complement and antibody to facilitate the binding of HIV-1 to CR2 in the absence of CD4 provides new insights into mechanisms of HIV-1-induced immunopathogenesis and infection-enhancement.
Clin Exp Immunol 1992 Dec
PMID:CD4-independent binding of HIV-1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody. 136 Aug 79


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