The virus causes measles, a highly contagious disease transmitted by respiratory aerosols that triggers a temporary but severe immunosuppression.

Symptoms include fever, cough, runny nose, inflamed eyes and a generalized, maculopapular, erythematous rash and a pathognomonic Koplik spot seen on buccal mucosa opposite to lower 1st and 2nd molars.

[2] The measles virus has two envelope glycoproteins on the viral surface – hemagglutinin (H) and membrane fusion protein (F).

[3] For wild type and vaccine strains, extracellular domains of CD150 (SLAM or SLAMF1)[4][5] and/or of nectin-4 (also called Poliovirus-Receptor-Like 4 (PVRL4))[6][7] mainly work as cell entry receptors.

The positive sense ssRNA is then mass translated by host ribosomes, producing all viral proteins.

The viruses are then assembled from their proteins and negative sense ssRNA, and the cell will lyse, discharging the new viral particles and restarting the cycle.

[12] 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.

The 450 nucleotides that code for the C‐terminal 150 amino acids of N are the minimum amount of sequence data required for genotyping a measles virus isolate.

Endemic transmission of measles virus was interrupted in the United States and Australia by 2000 and the Americas by 2002.