Description
Principle of the Assay: The microtiter plate provided in this kit has been pre-coated with MV. Samples are then added to the appropriate microtiter plate wells with a Horseradish Peroxidase (HRP)-conjugated MV-Ab-IgG and incubated. Then substrate solutions are added to each well. Only those wells that contain MV-Ab-IgG and enzyme-conjugated MV-Ab-IgG will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm.
Background: Measles virus (MV) is a single-stranded, negative-sense, enveloped RNA virus of the genus Morbillivirus within the family Paramyxoviridae. Humans are the natural hosts of the virus; no animal reservoirs are known to exist. The measles virus is the cause of measles, an infection of the respiratory system. Symptoms include fever, cough, runny nose, red eyes and a generalized,maculopapular, erythematous rash. The virus is highly contagious and is spread by coughing and sneezing via close personal contact or direct contact with secretions. The measles virus has two envelope glycoproteins on the viral surface - hemagglutinin (H) and membrane fusion protein (F). These proteins are responsible for host cell binding and invasion. Three receptors for the H protein have been identified to date: complement regulatory molecule CD46, the signaling lymphocyte activation molecule (SLAM) and the cell adhesion molecule Nectin-4. The measles virus evolved from the formerly widespread rinderpest virus, which infects cattle.[2] Sequence analysis has suggested that the two viruses most probably diverged in the 11th and 12th centuries, though the periods as early as the 5th century fall within the 95% confidence interval of these calculations. Other analysis has suggested that the divergence may be even older because of the technique's tendency to underestimate ages when strong purifying selection is in action. There is some linguistic evidence for an earlier origin within the seventh century.The current epidemic strain evolved at the beginning of the 20th century-most probably between 1908 and 1943