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)

The mechanisms of HIV infection of target cells are described. Particularly the role of three types of cell receptors, which participate in the process of virus-cell interactions: CD4 protein, receptor for Fc fragment of antibodies and complement receptors are discussed. The variability of the virus variants, which determines the virus tropism and cytotoxic properties towards specific cell types is stressed.
Pol Tyg Lek
PMID:[Mechanism of cell infection with HIV]. 823 49

Results of quantitative determinations of thrombocytes and selected, basal immune parameters in 263 HIV infected subjects are presented. A decrease in the platelet count was observed more frequently in symptomatic subjects, including AIDS patients, than in asymptomatic HIV carriers or patients with generalized lymphadenopathy only. A significant correlation between thrombocyte number and percentage and number of CD4+ lymphocyte and CD4+/CD8+ lymphocyte ratio was found only in the group of symptomatic subjects. The mechanisms responsible for thrombocytopenia in HIV infected patients ore discussed in details.
Pol Tyg Lek
PMID:[Appearance of thrombocytopenia in patients infected with HIV]. 823 50

Apoptosis is a mode of cell death defined by characteristic morphological, biochemical and molecular changes. It was first described as a "shrinkage necrosis", and then this term was replaced by apoptosis to emphasize its role opposite mitosis in tissue kinetics. During apoptosis the cell decrease in size, loose contact with neighboring cells, and loose specialized surface elements such as microvilli and cell-cell junctions. A shift of fluid out of the cells causes cytoplasm condensation, which is followed by convolution of the nuclear and cellular outlines. In later stages of apoptosis the entire cell becomes fragmented, forming a number of plasma membrane-bounded apoptotic bodies which contain nuclear and or cytoplasmic elements. The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane breakdown and cellular disintegration. Apoptosis occurs in many physiological and pathological processes. It plays an important role during embryonal development as programmed cell death and accompanies a variety of normal involutional processes in which it serves as a mechanism to remove "unwanted" cells. Apoptosis is associated with prostate atrophy after castration or atrophy of the adrenal cortex and thymus after administration of glucocorticoids. Apoptosis is involved in elimination of CD4 T lymphocytes in the course of HIV infection. The interest in apoptosis in oncology stems from the fact that it occurs in tumors, spontaneously as well as triggered by different antitumor drugs, radiation or after withdraw of growth factors. Spontaneous apoptosis may play a role in evolution of tumor malignancy.(ABSTRACT TRUNCATED AT 250 WORDS)
Patol Pol 1993
PMID:[Programmed death of cells (apoptosis)]. 824 38

40 asymptomatic HIV carriers and 45 AIDS patients were tested for anti-HBs (Hepatitis B Virus surface antigen), anti-RV (Rubella virus), anti-Toxo (Toxoplasma gondii), anti-CMV (Cytomegalovirus) and anti-HSV-1 (Herpes simplex virus type 1) antibody titers and compared with 83 persons characterized by risk behaviours but seronegative for HIV. The prevalence of these antibodies was very high and similar in all three groups studied, however, patients with AIDS had generally lower antibody titers when compared with asymptomatic carriers. The only exception being anti-HSV-1 which was present in high titre even in gravely ill patients. It seems that subjects with clinically overt HIV infection develop a serious disturbance in the humoral immune response with depressed specific antibody synthesis.
Pol Arch Med Wewn 1993 Aug
PMID:[Evaluation of humoral immune response in patients with asymptomatic and symptomatic HIV infection. Analysis of titers of anti-Hbs, antibodies against cytomegalovirus, herpes simplex virus type I, rubella virus and toxoplasma gondii]. 824 44

A primary HIV infection presenting as an acute viral syndrome in 31-years-old male drug addict is described. Two weeks after the probable infection the patient presented with fever, sweats, anorexia, vomiting, diarrhoea, myalgia, arthralgia, headaches, macular eruption, generalized lymphadenopathy, paresthesia and thrombocytopenia. These symptoms lasted 7 weeks. The immune abnormalities included an increase of CD8+ lymphocyte percentage resulting in decrease od CD4/CD8 ratio. HIV antigenemia was found 4 weeks after the presumed exposure whereas anti-HIV became detectable 2 weeks later.
Pol Arch Med Wewn 1993 Sep
PMID:[Concomitant symptom syndrome of primary HIV infection]. 828 48

It has been demonstrated that alveolar macrophages (AM) are permissive for human immunodeficiency virus (HIV-1) after in vitro infection. However, data concerning in vivo infection of AM by HIV-1 still conflict. Therefore, we investigated AM collected by bronchoalveolar lavage from 15 HIV-1-infected patients. HIV-1 p24 and Gp120 antigens and viral RNA were not detected by immunocytochemistry and in situ hybridization, respectively, using 35S-labeled 3 kb Pol-Env, 0.350 kb Gag, and 0.150 kb U5 LTR cRNA probes. In contrast, when using polymerase chain reaction on DNA extracted from purified AM, HIV-1 DNA was detected in the seven patients tested. After short-term culture of alveolar cells from three HIV-1-infected patients and in vitro stimulation with granulocyte/macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor-alpha (TNF-alpha), HIV-1 replication was observed in most of the AM. These results demonstrate that AM are latently infected by HIV-1 in vivo but are not a site for viral replication. In contrast, HIV-1 replication occurs when AM are withdrawn from their local environment, enhanced by GM-CSF and TNF-alpha stimulation. This suggests either a negative control or an inadequate stimulation of HIV-1 replication in the alveolar environment.
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PMID:HIV-1 in human alveolar macrophages from infected patients is latent in vivo but replicates after in vitro stimulation. 829 83

The integrase (IN) protein of HIV-1 was expressed as a processed and a non-processed protein in the eucaryotic baculovirus expression system. In immunoblots we could demonstrate that recombinant baculoviruses containing the complete gag and pol reading frames of HIV-1 expressed a gag/pol precursor polyprotein. The specific proteolytic activity of the recombinant protease on the gag and pol precursor proteins was used for the generation of processed gag (p 17, p 24, p 16) and pol (RT/RNaseH, IN) proteins. The non-processed IN protein, expressed as a polyhedrin fusion protein, was produced at much higher level than the processed protein.
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PMID:Expression of a processed and a non-processed form of the integrase protein of HIV-1 in the baculovirus system. 832 11

Bacteriological diagnosis of tuberculosis was performed in 104 HIV-positive patients, in majority AIDS patients hospitalized in AIDS Clinic of Infections and Parasitic Diseases Institute of Medical Academy. 390 samples were examined, e.d. 3.75 from each patient (from 1 to 22 samples). M. Tuberculosis was diagnosed in 14 patients and all of them were clinically observed because of pulmonary tuberculosis. The highest percentage of positive results was obtained from bronchial fluid evacuated during bronchoscopy.
Pneumonol Alergol Pol 1993
PMID:[Mycobacterial infection in patients with AIDS]. 834 94

The use of recombinant viruses for the expression of a wide array of foreign proteins has become commonplace during the last few years. Recently, we have described the construction and characterization of chimeric human immunodeficiency virus type 1 (HIV-1)-poliovirus genomes in which the gag and pol genes of HIV-1 have been substituted for the VP2 and VP3 capsid genes of the P1 capsid precursor region of poliovirus. Transfection of these RNAs into tissue culture cells results in replication of the RNA genome and expression of HIV-1-P1 fusion proteins (W. S. Choi, R. Pal-Ghosh, and C. D. Morrow, J. Virol. 65:2875-2883, 1991). Here we report on the encapsidation and amplification of the minireplicons to obtain sufficient quantities for biological characterization. To do this, HIV-1-poliovirus minireplicon genomes containing the gag or pol gene were transfected into cells previously infected with a recombinant vaccinia virus (VV-P1) which expresses the poliovirus capsid precursor protein, P1 (D. C. Ansardi, D. C. Porter, and C. D. Morrow, J. Virol. 65:2088-2092, 1991). The chimeric minireplicons replicated and expressed the appropriate HIV-1-P1 fusion proteins as determined by immunoprecipitation with HIV-1-specific antibodies. The encapsidated genomes were isolated by ultracentrifugation. Reinfection of cells with the encapsidated chimeric RNA genomes resulted in expression of the HIV-1-Gag-P1 or HIV-1-Pol-P1 fusion protein. Serial passaging of the encapsidated chimeric HIV-1-poliovirus genomes was accomplished by coinfecting cells with the encapsidated minireplicons and VV-P1, resulting in stocks of the encapsidated minireplicons. Northern (RNA) blot analysis of passaged material revealed that no detectable deletions of the chimeric genomes occurred during 14 serial passages. Infection of cells by the encapsidated minireplicons was blocked by antipoliovirus antibodies. Coinfection of cells with encapsidated minireplicons and type 1 Sabin poliovirus resulted in encapsidation of the chimeric genomes by wild-type poliovirus as measured by immunoprecipitation of the HIV-1-P1 fusion proteins with HIV-1-specific antibodies. The results of this study demonstrate the encapsidation of poliovirus minireplicons which express foreign proteins and point to the future use of this system as a potential vaccine vector.
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PMID:Encapsidation of genetically engineered poliovirus minireplicons which express human immunodeficiency virus type 1 Gag and Pol proteins upon infection. 838 2

The expression of the pol gene of human immunodeficiency virus type 1 (HIV-1) occurs by a ribosomal frameshift between the gag and the pol genes. The Gag-Pol polyprotein is produced at levels of 5 to 10% of that of the Gag protein, and is incorporated into virions to provide the viral protease, reverse transcriptase, and integrase which are essential for replication. The mechanism(s) by which the Gag-Pol polyprotein are targeted to the HIV virion is unknown, although it is believed to be via an interaction with the Gag protein. To further explore the mechanism by which the Gag-Pol polyprotein is incorporated into virions, we have constructed a mutation which changes an aspartic acid in the protease active site to asparagine (pHXB2pro-); a four-amino-acid insertion into the protease gene (pHXB2Smal); and insertion of translational termination codons in the protease gene following the gag gene (pHXB55). Transfection of these proviral genomes into COS-1 cells resulted in intracellular expression of only Pr55gag, demonstrating the inactivation of the viral protease. The expression of Pr55gag was evident in cells transfected with pHXB2pro- during a short pulse and first 3 hr of chase period, whereas at later times the intracellular levels of Pr55gag were greatly reduced. In contrast, the intracellular Pr55gag expressed from transfection of pHXB2Smal or pHXB55 were evident even after 6- or 12-hr chase times. To ascertain the effects of the mutations on the assembly and release of viruslike particles, the supernatants from the transfected cells were analyzed for the presence of Pr55gag. The release of Pr55gag from cells transfected with pHXB2pro- occurred as early as 1 hr following chase period, and increased for up to 3 hr. In contrast, reduced levels of Pr55gag were detected in the medium from cells transfected with pHXB2Smal or pHXB55. Subcellular fractionation studies demonstrated that the Pr55gag expressed from transfection of pHXB2pro- was rapidly targeted to intracellular membranes, while the majority of the Pr55gag expressed from transfection of pHXB2Smal or pHXB55 was distributed evenly between the cytoplasm and membrane fractions. Finally, the released viruslike particles obtained from the transfection of proviral genome pHXB2pro- were stable to mild detergent treatment, whereas particles obtained from transfection of pHXB2Smal and pHXB55 were relatively unstable. These results demonstrate that subtle changes in the Gag-Pol polyprotein of HIV-1 can have significant effects on the assembly and physical stability of the released virus.
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PMID:Mutations in the protease gene of human immunodeficiency virus type 1 affect release and stability of virus particles. 850 89


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