Measles virus is the only virus in this genus that causes disease in humans. Other viruses in the genus Morbillivirus are responsible for diseases in animals (for example, canine distemper virus). Measles virus differs in several ways from the other viruses in the family Paramyxoviridae.

1. Viral replication: The cellular receptor for measles virus is the CD46 molecule, a protein whose normal function is to bind certain components of complement. Although the viral attachment protein has hemagglutinating activity, it lacks neuraminidase activity. Hence, it is referred to as the H protein, rather than HN protein. An F protein facilitates uptake of the virion. Measles virus replication in tissue culture and certain organs of the intact organism is characterized by the formation of giant multinucleate cells (syncytium formation), resulting from the action of the viral spike F protein.

2. Pathology: Measles virus is transmitted by sneeze- or cough-produced respiratory droplets. The virus is extremely infectious, and almost all infected individuals develop a clinical illness. Measles virus replicates initially in the respiratory epithelium and then in various lymphoid organs. Classically, measles (previously referred to as rubeola) begins with a prodromal period of fever, cough, coryza (runny nose), and conjunctivitis (often referred to as the “3 C"s). Two to three days later, specific diagnostic signs develop. First, Koplik spots (small white spots on bright red mucous mem branes of the mouth and throat) appear (Figure 1), followed by a generalized macular rash, beginning at the head and traveling slowly to the lower extremities (Figure 2). Soon after the rash appears, the patient is no longer infectious. The major morbidity and mortality caused by measles are associated with various complications of infection, especially those affecting the lower respiratory tract and the CNS. The most important of these is postinfectious encephalomyelitis, which is estimated to affect 1 of 1,000 cases of measles, usually occurring within 2 weeks after the onset of the rash. This is an autoimmune disease associated with an immune response to myelin basic protein. Figure 3 shows the time course of measles virus infection. Children are particularly susceptible, especially those weakened by other diseases or malnutrition. Measles is, therefore, an important cause of child hood mortality in developing countries.

Fig1. Koplik spots in the mouth caused by measles virus.

Fig2. The measles rash consists of large, slightly raised lesions called maculopapules. These run into each other to form irregular blotches.

Fig3. Time course of measles virus infection.

3. Diagnosis: In most cases, there is little difficulty in making a diagnosis of measles on clinical grounds, especially in an epidemic situation. The presence of Koplik spots provides a definitive diagnosis. If a laboratory diagnosis is necessary, it is usually made by demonstrating an increase in the titer of antiviral antibodies.

4. Prevention: Measles is usually a disease of childhood and is followed by lifelong immunity. A live, attenuated measles vaccine, which has been available for many years, has greatly reduced the incidence of the disease. Nevertheless, occasional outbreaks of measles continue to occur, especially in older children and young adults, possibly due to waning immunity. Thus, two doses of the vaccine, in the form of the measles-mumps-rubella (MMR) vac cine, are now recommended, the first at 12 to 18 months, the second at 4 to 6 years. Parental resistance to the MMR vaccine has led to populations of children who are susceptible to measles. Importation of the virus by returning international travelers has led to recent outbreaks in the United States among unvaccinated children.

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مواضيع ذات صلة

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Rubeola (Measles)

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Human T-cell Lymphotropic Viruses, Types 1 and 2

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Congenital Rubella Infection

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Acute and Chronic Hepatitis C

Hepatitis C

Pathogenesis and clinical significance of HIV