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What causes measles?
Last reviewed: 04.07.2025

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The causative agent of measles is a large virus with a diameter of 120-250 nm, belongs to the Paramyxoviridae family, genus Morbillivirus.
Unlike other paramyxoviruses, the measles virus does not contain neuraminidase. The virus has hemagglutinating, hemolytic and symplast-forming activity.
Pathogenesis of measles
The entry point for the virus is the mucous membranes of the upper respiratory tract. There are indications that the conjunctiva of the eye may also be an entry point for infection.
The virus penetrates the submucosa and lymphatic tract of the upper respiratory tract, where its primary reproduction occurs, then enters the blood, where it can be detected from the first days of the incubation period. The maximum concentration of the virus in the blood is observed at the end of the prodromal period and on the 1st day of the rash. During these days, the virus is present in large quantities in the discharge of the mucous membranes of the upper respiratory tract. From the 3rd day of the rash, the excretion of the virus decreases sharply and is not detected in the blood. Virus-neutralizing antibodies begin to predominate in the blood.
The measles virus has a special tropism for the central nervous system, respiratory tract, and gastrointestinal tract. It has now been established that the measles virus can persist in the brain for a long time and cause chronic or subacute infection. Subacute sclerosing panencephalitis is also associated with persistent measles infection.
The appearance of a rash on the skin should be considered as a result of fixation of immune complexes in the skin vessels, formed during the interaction of viruses, antigens with antibodies. The epidermal cells are degenerated, necrotic, and then in the affected areas there is increased keratinization of the epidermis with subsequent rejection (peeling). The same inflammatory process occurs on the mucous membranes of the oral cavity. The degenerated and then keratinized epithelium becomes cloudy, rises, forming small whitish foci of superficial necrosis (Filatov-Koplik spots).