Disease relevance of Measles Virus

• SSPE and MS patients had a higher antibody activity towards measles virus than controls [1].
• A radiolabelled 50-base oligonucleotide complementary with the measles virus gene encoding the nucleocapsid was used as a probe to identify persistent measles virus genome in the lymphocytes from patients with autoimmune chronic active hepatitis (AICAH) [2].
• Vaccinia virus recombinants encoding the hemagglutinin or fusion protein of measles virus have been constructed [3].
• The monoclonal antibody against measles virus phosphoprotein did not react with herpes simplex virus protein and vice versa, indicating that these monoclonal antibodies recognize different antigenic determinants on the intermediate filament molecule [4].
• Age-matched serum and cerebrospinal fluid from 20 multiple sclerosis patients and 20 control patients with other neurological diseases were examined for antibodies to radiolabeled measles virus and canine distemper virus using an immunoprecipitation polyacrylamide gel technique [5].

High impact information on Measles Virus

• A study of lymphocyte markers suggested that the complement regulator known either as membrane cofactor protein or CD46 was the measles virus receptor [6].
• The measles virus (MV) phosphoprotein (P) gene encodes two known proteins, P (Mr approximately 70,000), involved in viral transcription, and, in a different reading frame, C (Mr approximately 20,000) [7].
• Measles virus editing provides an additional cysteine-rich protein [7].
• These fixatives and the removal of the measles virus hemagglutinin from the cell surface by trypsin enabled studies of the appearance of the hemagglutinin at the surface membrane [8].
• Fixation with glutaraldehyde (GA) and paraformaldehyde (PFA) preserved measles virus hemagglutinin at the surface of chronically infected cells [8].

Chemical compound and disease context of Measles Virus

• PFA fixation, in contrast to GA fixation, also preserved the immunogenicity of measles virus hemolysin [8].
• Here we show that human SLAM (signalling lymphocyte-activation molecule; also known as CDw150), a recently discovered membrane glycoprotein expressed on some T and B cells, is a cellular receptor for measles virus, including the Edmonston strain [9].
• In this report, we demonstrate that measles virus (MV) replicates weakly in the resting dendritic cells (DC) as in lipopolysaccharide-activated monocytes, but intensively in CD40-activated DC [10].
• When lymphocytes from patients with measles or when normal cells infected with measles virus in vitro were treated with either levamisole or L-ascorbic acid for 15 min and then retested with the OKT antisera, restoration of the previously depleted OKT3+ and OKT4+ cell population was observed [11].
• However, the safety and value of giving vitamin A, a potent immune enhancer, with live measles virus vaccines are unknown [12].

Biological context of Measles Virus

• Efficient major histocompatibility complex class II-restricted presentation of measles virus relies on hemagglutinin-mediated targeting to its cellular receptor human CD46 expressed by murine B cells [13].
• Mice vaccinated with a single dose of the recombinant encoding the hemagglutinin protein developed antibodies capable of both inhibiting hemagglutination activity and neutralizing measles virus, whereas animals vaccinated with the recombinant encoding the fusion protein developed measles neutralizing antibodies [3].
• Patient brain-derived RNA, subjected to reverse transcription followed by polymerase chain reaction yielded polymerase chain reaction products with measles virus but not parainfluenza virus genes [14].
• Membrane cofactor protein (MCP, CD46), a widely distributed regulatory protein, inhibits complement activation on host cells and serves as a measles virus receptor [15].
• We demonstrated that expression of the hemagglutinin (H) protein of measles virus was sufficient for down regulation [16].

Anatomical context of Measles Virus

• In these studies, a number of human cell lines including epithelial, neural, glial, and lymphoid cells infected with several strains of measles virus were found to be lysed upon incubation with fresh sera from humans containing antibody measles virus [17].
• Signaling lymphocyte activation molecule (SLAM), a glycoprotein expressed on activated lymphocytes and antigen-presenting cells, has been shown to be a coregulator of antigen-driven T cell responses and is one of the two receptors for measles virus [18].
• Purified hemagglutinin and fusion glycoproteins of measles virus either in soluble form or inserted in artifical membranes bind to human peripheral blood lymphocytes and induce cell-mediated cytotoxicity (CMC) in a dose-response fashion [19].
• Third, infection of HeLa cells by measles virus greatly increased their susceptibility to NK lysis but produced no change in surface transferrin receptor expression [20].
• In contrast, measles virus infection induced CSA production by passaged endothelial cells even in the absence of MCM [21].

Gene context of Measles Virus

• The human CD46 molecule is a receptor for measles virus (Edmonston strain) [6].
• Measles virus induced MCP-1 and MCP-2 in most cell types [22].
• Hemagglutinin protein of wild-type measles virus activates toll-like receptor 2 signaling [23].
• Recognition of the measles virus nucleocapsid as a mechanism of IRF-3 activation [24].
• Here we demonstrate that measles virus can inhibit cytokine responses by direct interference with host STAT protein-dependent signaling systems [25].

Analytical, diagnostic and therapeutic context of Measles Virus

• Disruption of Akt kinase activation is important for immunosuppression induced by measles virus [26].
• Sequence analysis of measles virus nucleocapsid transcripts in patients with Paget's disease [27].
• Antibodies that were retrieved reacted strongly with measles virus cell extracts by enzyme-linked immunosorbent assay and were specific for the measles virus nucleocapsid protein [28].
• Transgenic expression of a CD46 (membrane cofactor protein) minigene: studies of xenotransplantation and measles virus infection [29].
• Neonatal and maternal sera were assessed by nephelometry for total levels of serum IgG and by ELISA for IgG antibodies to herpes simplex virus (HSV), varicella-zoster virus (VZV), measles virus, tetanus toxoid, streptolysin O, and Streptococcus pneumoniae capsular antigens [30].

References