Morphology and Structure
The measles virus is spherical with a diameter of approximately 150 nm. In the center lies the nucleocapsid, which contains RNA bound to the nucleoprotein (N), phosphoprotein (P), and polymerase (L).
Enveloping the capsid is a lipid bilayer studded with glycoprotein spikes:
- Hemagglutinin (H) — mediates viral adsorption to the host cell.
- Fusion protein (F) — induces the fusion of cell membranes, forming multinucleated giant cells (syncytia), and exhibits hemolytic activity.
Beneath the envelope lies the matrix (M) protein, which participates in virion assembly. Unlike many other paramyxoviruses, the measles virus lacks neuraminidase. The pathogen shares common antigens with canine distemper virus and rinderpest virus.
Stability and Epidemiology
The virus is extremely labile in the environment. It is rapidly inactivated by sunlight, UV radiation, and room temperature (within 3–4 hours). The presence of a lipoprotein envelope makes it sensitive to detergents and disinfectants.
Measles is an anthroponosis; humans are the only reservoir and source of infection. The disease is distributed globally, and susceptibility is nearly 100%. The primary transmission route is airborne droplets. Infectivity peaks during the prodromal period and the first day of the rash. Five days after the appearance of the rash, the patient is no longer considered infectious.
Pathogenesis and Clinical Features
Upon entering through the respiratory mucosa and conjunctiva, the virus infects regional lymph nodes before entering the bloodstream (primary viremia). It then replicates within cells of the reticuloendothelial system, followed by a secondary, more massive release of the pathogen into the bloodstream (secondary viremia). The virus targets capillary endothelium, causing edema, necrosis, and the characteristic rash.
The clinical presentation includes:
- Prodromal (catarrhal) phase: fever, rhinitis, pharyngitis, and conjunctivitis with photophobia.
- Pathognomonic sign: one day before the rash appears, Koplik spots (small bluish-white spots with a erythematous base) develop on the buccal mucosa.
- Eruptive phase: a maculopapular rash that spreads in a cephalocaudal direction (face $\rightarrow$ trunk $\rightarrow$ extremities).
The illness lasts 7–9 days, and the rash fades leaving brownish hyperpigmentation.
Immunity and Complications
The measles virus suppresses T-lymphocyte activity, predisposing patients to secondary bacterial infections such as pneumonia and otitis media. Following recovery, durable, lifelong humoral immunity is established. Newborns are protected by maternal IgG during the first 6 months of life.
A rare but fatal complication is subacute sclerosing panencephalitis (SSPE), a slow virus infection. It arises from the persistence of defective virions (featuring mutated F proteins and a lacking M protein) within neuroglial cells. SSPE is characterized by neuronal death, severe neurological deterioration, and extraordinarily high antibody titers in serum and cerebrospinal fluid.
Diagnostics and Prevention
Diagnostics utilize nasopharyngeal swabs, blood, urine, and skin scrapings. The virus can be cultured in cell lines, where it induces syncytium formation. Additional methods include RT-PCR, direct immunofluorescence (DFA) for rapid diagnostics, and serology (CF, HI, ELISA).
The primary method of prevention is routine vaccination with a live attenuated vaccine (monovalent or combination) administered at 1 year of age. In outbreak settings, non-immune, vulnerable children may receive normal human immunoglobulin (administered no later than the 7th day of the incubation period).