Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021311 (Infection)
38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of Human organism by Human Immunodeficiency viruses induces, after a shorter or a longer period, a complex immune Deficiency (ID) that has been named Acquired Immune Deficiency Syndrome (AIDS). Although the designation is not correct, it has been accepted by the scientific community. AIDS includes multiple clinical situations that have in common HIV infection and an almost constant ID, that at the end of natural course of infection manifestated by the presence of opportunistic infections and malignant tumors. HIV-1 and HIV-2 are slow RNA viruses with a common architecture and well known genomic organization. The characteristics that made HIV infectious agent n. 1 in XXth Century are their remarkable heterogeneity, close AA sequence homology between some of their proteins and relevant molecules in human beings: MHC molecules, IL-2, VIP, etc. and a strong affinity of gp 120 to CD4 receptor of T helper lymphocytes (T4), mononuclear phagocytes, natural killer cells, etc. all of them sharing a relevant role in normal immune response (IR). Affected in its cornerstones of cellular defense, human organism starts an immune defense through antibodies, cytotoxic T Lymphocytes (CTL) Natural Killer Cells (NK) antibody dependent cell cytotoxicity (ADCC), that fails. Activating immune system HIV turn that defense strategy to their own profit and enhanced replication. After an apparent latency period--in which the balance seems to favor the host--new viral variants arise due to high rate of HIV mutagenesis, that in turn stimulate immune system, induce new cycles of viral replication and new high virulent mutants, leading to the final collapse of Immune System.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunologic aspects of HIV infection]. 180 34

Oocysts of cryptosporidia whose morphology and measurements corresponded with those of the species Cryptosporidium baileyi were found in the stool of an immunodeficient patient. In autopsy material, cryptosporidia were found in the esophagus, whole intestine, trachea, larynx, lungs, and gall and urinary bladders. None of the 69 suckling mice inoculated with this isolate developed cryptosporidial infection. Infection was successful in 26 chickens inoculated perorally and 6 others subjected to intratracheal inoculation; it was localized in the duodenum, jejunum, bursa Fabricii, and respiratory tract. From day 12 after infection, oocysts of cryptosporidia were found in the excrement. Human infection with C. baileyi may have occurred due to disruption of the immune system by human immunodeficiency virus (HIV) and to immunosuppressive therapy undertaken after allogeneic kidney transplantation.
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PMID:The first finding of Cryptosporidium baileyi in man. 182 38

Incubation of the human T cell lymphotropic virus (HTLV)-IIIB and HTLV-RF strains of human immunodeficiency virus type 1 (HIV-1) with normal seronegative human serum under conditions that allow complement activation resulted in enhancement of infection of the MT2 human T cell line cultured in the presence of low amounts of virus. Infection of MT2 cells was assessed by measuring reverse transcriptase activity in supernatants at day 9 of culture. Complement activation by viral suspensions occurred through the alternative pathway. Opsonization of HTLV-RF viral particles with complement was sufficient to allow a productive infection to occur in cells exposed to suboptimal amounts of virus. Infection of MT2 cells with suboptimal amounts of serum-opsonized HIV-1 was suppressed by blocking the C3dg receptor (CR2, CD21) on MT2 cells with monoclonal anti-CR2 antibody and rabbit F(ab')2 anti-mouse immunoglobulin antibodies. Blocking of the gp120-binding site on CD4 under similar experimental conditions had no inhibitory effect on infection of MT2 cells with opsonized virus. Opsonization of HIV-1 with seronegative serum also resulted in a CR2-mediated enhancement of the infection of normal peripheral blood mononuclear cells and T lymphocytes. These results indicate that complement in the absence of antibody may enhance infection of C3 receptor-bearing T cells with HIV-1, and that the interaction of opsonized virus with the CR2 receptor may result by itself in the infection of target T cells in a CD4- and antibody-independent fashion.
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PMID:Complement mediates human immunodeficiency virus type 1 infection of a human T cell line in a CD4- and antibody-independent fashion. 182 39

Human immunodeficiency virus (HIV) complexed with human anti-HIV IgG can attach to Fc gamma receptors (Fch) of mononuclear phagocytes. To determine whether the FcR-mediated infection that results also requires interaction between HIV gp120 and cell membrane CD4, monocytic cells of the U937 line were transiently treated with phorbol 12,13-dibutyrate (PDB) so that they temporarily presented a CD4-FcR+ phenotype at the time of HIV infection. HIV production was not abolished, but only significantly delayed after infection of these cells with free virus. Leu3a monoclonal antibody or soluble recombinant CD4 completely blocked this delayed infection. This indicates that enough CD4 still remained at the membrane to allow infection of a reduced cell number. Infection of PDB-treated cells with virus preincubated with high anti-HIV IgG concentrations was inhibited, contrasting with what was observed with control cells infected under the same conditions. Inhibition of infection was also observed when HIV became attached to untreated U937 cells through the binding of CD4-IgG hybrid molecules to FcR. Thus, the binding of IgG-coated virus to FcR is not sufficient in itself to elicit productive infection of monocytic cells, which still requires the interaction of viral gp120 and membrane CD4.
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PMID:Infection of monocytic cells by HIV1: combined role of FcR and CD4. 183 82

Infection with human herpesvirus 6 (HHV-6) was found to up-regulate expression of human immunodeficiency virus and human T cell leukaemia virus type I (HTLV-I) long terminal repeat sequence (LTR), and herpes simplex virus type 1 (HSV-1) gD chloramphenicol acetyltransferase (CAT) constructs transfected into the T cell line, J. Jhan. Activation by HHV-6 was due to one or more viral proteins produced early in infection and, in the case of the HTLV-I LTR, was synergistic to induction mediated by the HTLV-I tax gene product. Neither the HTLV-I enhancer nor basal promoter elements of the HSV-1 gD gene were essential for activation and no increase in accumulated HTLV-I mRNA was observed due to HHV-6 infection. Induction by HHV-6 was found to be dependent on the reporter construct used, because the CAT gene and, to a lesser extent, the HSV-1 thymidine kinase gene were responsive to HHV-6 infection although no significant activation of growth hormone constructs was observed. Our results bear a strong resemblance to those obtained for the Epstein-Barr virus BMLF1 gene, indicating that the major HHV-6 trans-activator may be a homologue of this gene.
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PMID:Activation of gene expression by human herpesvirus 6 is reporter gene-dependent. 185 12

Immunization with an inactivated whole-virus vaccine is highly effective in preventing lentivirus infection. The viral protein(s) essential to the induction of protective responses, however, have not been identified. To define the role of virion components in the induction of protective immunity, we evaluated the efficacy of glycoprotein-enriched and glycoprotein-depleted simian immunodeficiency virus (SIV) subunit vaccines prepared by lentil-lectin affinity chromatography of gradient-purified virions using the immunization and challenge regimen previously found successful with an inactivated whole-virus vaccine. Infection was determined by successful recovery of virus, the induction of SIV-specific antibody responses, and infection of naive recipients by inoculation with lymph-node-derived lymphocytes from the vaccinates. Immunization with the glycoprotein-enriched preparation prevented infection in two out of four monkeys, whereas the glycoprotein-depleted vaccine failed to prevent infection in all four vaccinates tested. However, the glycoprotein-depleted vaccine appeared to moderate the progression of SIV-induced disease compared with non-immunized infected control monkeys inoculated with the same challenge dose. These data suggest that subunit vaccines containing sufficient quantities of viral glycoproteins can protect against SIV infection, whereas subunit vaccines composed predominantly of viral core proteins cannot. The development of effective vaccines against HIV infection should include studies on the optimum presentation of the viral envelope glycoproteins to produce long-term broadly protective immune responses.
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PMID:Efficacy of SIV/deltaB670 glycoprotein-enriched and glycoprotein-depleted subunit vaccines in protecting against infection and disease in rhesus monkeys. 188 40

CD4 is an integral cell surface glycoprotein that is able to enhance T cell specific antigen responses when it interacts with its physiological ligand, class II major histocompatibility (MHC) molecules. In addition, CD4 is a specific cell-surface receptor for the human immunodeficiency virus-1 (HIV-1). Infection by HIV-1 is initiated by the binding of the envelope glycoprotein, gp120, to the first domain of CD4. The binding of CD4 to class II MHC is inhibited by gp120, one possible mechanism for immunosuppression in AIDS patients. In addition, the CD4/gp120 interaction may directly inhibit T cell function. Recently we have synthesized small molecules (CPFs) that specifically inhibit this interaction. CPFs bind to gp120 and prevent the binding of gp120 to CD4, and also inhibit the infectivity of HIV-1.
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PMID:The interaction of CD4 with HIV-1 gp120. 188 98

The prevalence of human T-cell leukaemia virus-I and -II infection was studied in a cohort of 346 intravenous and nonintravenous drug users in Amsterdam. Three participants (0.86%) had antibodies to HTLV-I by two commercially available HTLV-I enzyme immunoassays (EIA). Infection in these three subjects was confirmed by radioimmunoprecipitation assay. In the immunoblot study, only two of the three subjects were considered positive, since the serum of the third subject had antibodies to p24 only. By means of the polymerase chain reaction two participants (male intravenous drug users infected with human immunodeficiency virus; HIV) appeared to be infected with HTLV-I and one subject (a male nonintravenous drug user from Surinam) with HTLV-II. It is concluded that HTLV-I and HTLV-II circulate sporadically among drug users in Amsterdam and that risky injecting behaviour, which led to an HIV epidemic among intravenous drug users, has not led so far to an appreciable transmission of the other retroviruses among this group.
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PMID:Low prevalence of human T-cell leukaemia virus-I and -II infection among drug users in Amsterdam, The Netherlands. 189 Apr 9

Peripheral blood cells were obtained from patients at different stages of their human immunodeficiency virus (HIV) infection. It was found that the capacity to generate interferon alpha was reduced already at Walter Reed stage 2 (WR) while the interferon gamma capacity remained largely unaffected until WR stage 4. Endogenous tumor necrosis factor (TNF) alpha production increased as the HIV disease progressed. The data obtained add to our knowledge on destruction of the immune system by the HIV. Moreover TNF and acid labile interferon alpha might contribute to HIV replication and disease progression. Nevertheless the tests performed are too time-consuming to be introduced into routine analysis of HIV infection or for monitoring its therapy and can so far not be used for intervention strategies. Further studies are needed.
Infection 1991
PMID:Tumor necrosis factor and interferon as prognostic markers in human immunodeficiency virus (HIV) infection. 190 34

Infection due to the human immunodeficiency virus (HIV) has been complicated by the development of acute nonlymphocytic leukemia in five patients whose cases have previously been reported; other manifestations, including preleukemia, myelofibrosis, and myeloid hyperplasia, have also been reported in patients infected with HIV. We report the sixth case of an HIV-infected patient who developed acute myelomonocytic leukemia; HIV infection was documented by tests for serum antibodies (enzyme-linked immunosorbent assay and western blotting), by a markedly elevated p24 antigen level in plasma, and by cultures of CSF and peripheral blood that were positive for HIV. Furthermore, myelomonoblasts that were cultured without the addition of growth factors displayed evidence of HIV replication through the presence of p24 antigen and reverse transcriptase activity, both of which lasted for 4 weeks in the supernatant fluid of the cell cultures. This case report provides the first data indicating that HIV may infect myelomonoblasts in vivo and represents the sixth reported case of an association between HIV infection and pure acute nonlymphocytic leukemia.
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PMID:Relationship between acute myelomonoblastic leukemia and infection due to human immunodeficiency virus. 190 61


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