Disease relevance of Hemadsorption

• Identification of two amino acids in the hemagglutinin glycoprotein of measles virus (MV) that govern hemadsorption, HeLa cell fusion, and CD46 downregulation: phenotypic markers that differentiate vaccine and wild-type MV strains [1].
• The DVIM strain of MHV expresses large amounts of HE glycoprotein, as shown by hemadsorption, acetylesterase activity, and immunoreactivity with antibodies directed against the HE glycoprotein of bovine coronavirus [2].
• The Vsa proteins modulate susceptibility of Mycoplasma pulmonis to complement killing, hemadsorption, and adherence to polystyrene [3].
• Clinicians should be aware that parainfluenza virus type 3, one of the most common causes of viral respiratory infection in infancy, can also produce infection of the CNS and that hemadsorption testing of CSF specimens submitted for viral culture is necessary for detecting these paramyxoviruses [4].
• An African swine fever virus gene with similarity to the T-lymphocyte surface antigen CD2 mediates hemadsorption [5].

High impact information on Hemadsorption

• Cells fixed with PFA but not with GA exhibited hemadsorption with green monkey cells [6].
• Immune adherence, protein A, and C3-mixed hemadsorption assays detected reactivity in a high percentage of patients (80-100%), whereas mixed hemadsorption assays were negative with sera from all but one patient [7].
• Quantitative absorption experiments in the mixed hemadsorption assay determined that the expression of MAA and beta 2m on treated cells was enhanced at 10(2)-10(5) U IFN/ml, twofold to fivefold for MAA and fivefold to twelvefold for beta 2m [8].
• After short-term culture in vitro, however, cells from all three types of tissue were only weakly agglutinated by Con A, as measured by both suspension and hemadsorption assays [9].
• Positive reactions ranged from 12 to 32% in mixed hemadsorption for anitbody detection and from 10 to 34% in mixed hemadsorption for complement component 3 detection [10].

Biological context of Hemadsorption

• The converse double mutagenesis of the Ma93F H protein (E451V/N481Y) transferred the CD46-downregulating, fusogenic, and hemadsorption functions to this protein [1].
• SPI-3-negative strains fused despite the fact that the HA was expressed and processed normally, i.e., cells infected with SPI-3 mutants remained functionally hemadsorption positive, and analysis of the HA protein by Western immunoblot suggested that posttranslational modifications of the HA protein appeared normal [11].
• Specific IgM-positive sera showed hemadsorption, whereas negative sera showed hemagglutination [12].
• These results indicate that sialic acid on oligosaccharides near the receptor binding site interferes with hemadsorption [13].
• The G protein expressed by the recombinant CHV was processed and transported to the cell surface as in RV infected cells, and showed the same biological activities such as low pH dependent cell fusion and hemadsorption [14].

Anatomical context of Hemadsorption

• Cells expressing C28a HN did not bind erythrocytes at 4 degrees C unless pretreated with neuraminidase, but no such pretreatment was required for hemadsorption activity (HAD) at 22 or 37 degrees C. HAD was blocked by 4-GU-DANA, attesting to the ability of this compound to inhibit HN's receptor-binding activity [15].
• The former downregulate CD46, the putative cellular receptor of MV, are positive for hemadsorption, and are fusogenic in HeLa cells, whereas the latter are negative for these phenotypic markers [1].
• Focal syncytia were formed containing measles antigen and accumulations of nucleocapsid-like structures with no detectable production of transmissible infectious virus or positive hemadsorption [16].
• The results of an in vitro mixed hemadsorption (MHA) assay predicted the success of in vivo tumor localization using a radioiodinated, monoclonal, IgG1 antibody (A2) with reactivity to the human bladder carcinoma cell line RT4 [17].

Associations of Hemadsorption with chemical compounds

• The order-of-magnitude lower 50% inhibitory concentrations of 4-GU-DANA (and also DANA and 4-AM-DANA) for plaque area reduction and for inhibition in the fusion assay than for reducing plaque number or blocking hemadsorption indicate the particular efficacy of these sialic acid analogs in interfering with cell-cell fusion [18].
• Treatment of BGM/MV cells with 5-bromo-2'-deoxyuridine (BUdR) at 5 to 50 mug/ml and cytosine arabinoside at 1 to 50 mug/ml failed to enhance hemadsorption activity [19].
• The hemadsorption activity of the cells could be enhanced (30 to 70%) by treatment with actinomycin D or enucleation with cytochalasin B; these treatments, however, were unsuccessful in inducing detectable levels of measles hemagglutinin [19].
• These methods are based on mannose-resistant hemadsorption or CFA enzyme-linked immunosorbent assay (ELISA) on nitrocellulose replicas of the cultures allowing simultaneous analysis of up to 200 colonies per plate [20].
• Gangliosides partially inhibited fusion and hemadsorption, but not neuraminidase hemagglutinin-neuraminidase glycoprotein (HN) activity [21].

Gene context of Hemadsorption

• Moreover, in the hemagglutinin gene of a strain showing strongly reduced hemadsorption, 20 clustered A to G mutations, resulting in 16 amino acid changes, were detected [22].
• Sera from all mice were screened for reactivity to Meth A by complement-dependent cytotoxicity, protein A, and mixed hemadsorption assays [23].
• SLE sera were screened for the presence of surface neuronal antibodies using a mixed hemadsorption assay [24].
• The hemadsorption and neuraminidase activities of the chimeric viruses showed significant differences from those of their parental strains, but heterotypic F and HN pairs were equally effective in fusion promotion [25].
• Otherwise, the presence of the heterologous transmembrane and cytoplasmic domains had little effect on the processing of the HN or G ectodomain, as assayed by the acquisition of N-linked and O-linked carbohydrates, transport to the cell surface and, in the case of HN, folding, oligomerization, and hemadsorption activity [26].

Analytical, diagnostic and therapeutic context of Hemadsorption

• Paired sera from 763 children and adults admitted to the hospital for acute respiratory disease were tested for significant antibody titer rises in the hemagglutination inhibition (HI) test and for specific IgM antibody with the hemadsorption immunosorbent techniques (HIT) [27].
• The increase in hemadsorption is accompanied by an alteration in distribution of receptors within the cell population as measured by flow microfluorometry using fluorescin conjugated concanavalin A, and by a decrease in the total number of receptors as measured by binding of radiolabelled concanavalin A [28].
• Site-directed mutagenesis of the H genes were performed to confirm that the substitution of Ser --> Gly at position 546 and Asn --> Tyr at position 481 in the H protein were responsible for hemadsorption alteration [29].

References