Morphology and structure
The measles virus is spherical with a diameter of about 150 nm. In the center is the nucleocapsid containing RNA associated with the nucleoprotein (N), phosphoprotein (P), and polymerase (L).
A viral envelope (supercapsid) with glycoprotein spikes is located on the outside:
- Hemagglutinin (H) — ensures virion adhesion to the cell.
- Fusion protein (F) — causes the fusion of cell membranes with the formation of multinucleated cells (symplasts) and exhibits hemolytic activity.
Beneath the supercapsid lies the matrix protein (M), 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.
Resistance and Epidemiology
The virus is extremely unstable in the external environment. It is rapidly destroyed by sunlight, UV rays, and room temperature (within 3–4 hours). The presence of a lipoprotein envelope makes it sensitive to detergents and disinfectants.
Measles is an anthroponosis; the only source of infection is a sick person. The disease is widespread globally, and susceptibility to it is close to 100%. The main transmission route is airborne. Maximum contagiousness is observed during the prodromal period and on the first day of the rash. Five days after the appearance of the rash, the patient ceases to be a source of infection.
Pathogenesis and clinical features
Penetrating through the mucous membranes of the respiratory tract and conjunctiva, the virus enters regional lymph nodes and then the blood (primary viremia). Next, it multiplies in the cells of the reticuloendothelial system, after which a secondary, more massive release of the pathogen into the bloodstream occurs (secondary viremia). The virus damages the capillary endothelium, causing edema, necrosis, and the characteristic rash.
The clinical picture includes:
- Catarrhal stage: fever, rhinitis, pharyngitis, conjunctivitis with photophobia.
- Pathognomonic sign: a day before the rash, Koplik's spots (small whitish-gray elements with a red halo) appear on the buccal mucosa.
- Stage of rash: maculopapular rash spreading from top to bottom (face $\rightarrow$ trunk $\rightarrow$ extremities).
The disease lasts 7–9 days; the rash disappears, leaving behind pigmentation.
Immunity and complications
The measles virus suppresses T-lymphocyte activity, which contributes to the development of secondary bacterial infections (pneumonia, otitis media). After the disease, a persistent, lifelong humoral immunity is formed. 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 viral infection. It occurs due to the persistence of defective virions (with an altered F-protein and lacking the M-protein) in the neuroglia. SSPE is characterized by neuronal loss, severe neurological disorders, and extremely high antibody titers in the blood and CSF.
Diagnostics and prevention
Diagnostics utilize nasopharyngeal swabs, blood, urine, and rash scrapings. The virus is cultured in cell lines, where it induces symplast formation. PCR, DFA (for rapid diagnostics), and serological methods (CF test, HI test, ELISA) are also used.
The primary method of protection is routine vaccination with a live attenuated vaccine (monovalent or combined) at 1 year of age. In infection foci, unvaccinated immunocompromised children are administered normal human immunoglobulin (no later than the 7th day of the incubation period).
The sequential appearance of the measles rash is easy to remember by the "top-to-bottom" rule: it first erupts on the face, the next day on the trunk, and then on the extremities.
Class and exam questions
What is the pathognomonic symptom of measles?
These are Koplik spots (Belsky–Filatov–Koplik spots) — small whitish-gray spots with a red halo on the buccal mucosa that appear a day before the skin rash.
What is SSPE and how does it develop?
Subacute sclerosing panencephalitis is a fatal slow CNS infection. It is associated with the prolonged persistence of defective measles virus forms in neuroglial cells.
How does the measles virus affect the immune system?
The measles virus causes pronounced immunosuppression by suppressing T-lymphocytes, which increases the risk of secondary bacterial flora.
What type of immunity is formed after contracting measles?
Persistent, generally lifelong humoral immunity is formed. Relapses are extremely rare.
What else to study on this topic
- Mechanism of symplast formation induced by the F-protein
- Similarities between the measles virus and canine distemper virus and its significance
- Features of defective virion formation in SSPE
- Principles of laboratory diagnostics for measles
- Specific and emergency prophylaxis of the infection
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