Measles virus: structure, pathogenesis, clinical feature, complications and lab diagnosis

The name measles is derived from the Latin, misellus, meaning miserable.

  • Measles (also called Rubeola-(from rubeolus, Latin for reddish) ) is usually a disease of childhood (aged 3-10 years) and is followed by life-long immunity.
  • Important cause of childhood  mortality in developing countries.
  • Human is the natural host

Structure of Measles Virus

  • Measles virus is a member of the genus Morbillivirus of the family Paramyxoviridae. Paramyxoviruses are so called because they have an affinity for mucous membranes (Greek: myxa = mucus).

    Structure of Measles Virus
    Structure of Measles Virus
  • Measles virus is a typical paramyxovirus (spherical enveloped particles that contain a non segmented negative strand RNA genome with a linear arrangement of genes)
  • Measles virus have two glycoproteins  spikes that are important in pathogenesis:
    • F (fusion) protein, which is responsible for fusion of virus and host cell membranes, viral penetration, and haemolysis, and the
    • H (haemagglutinin) protein, which is responsible for binding of virus to cells
  • Measles virus has only one serotype i.e. Life long immunity occurs in individuals who have had the disease.
  • Hemagglutinin is the antigen against which neutralizing antibody is formed.
  • Infants are protected during the first six months of life ( they get maternal antibody as it passes the placenta)

Replication cycle of Measles Virus

  • Adsoprtion to the cell surface: via Hemagglutinin. Cellular receptor of measles virus is CD46 molecule.
  • Penetrates the cell surface and uncoats
  • Virion RNA polymerase transcribes the negative-strand genome to mRNA
  • Specific viral proteins are formed
  • Assembly to helical nucleocapsid
  • Release of virus by budding

Transmission and Epidemiology of Measles

  • Worldwide distribution, outbreaks in 2-3 years
  • Measles virus is extremely infectious, most children contract clinical disease on exposure
  • Transmitted via respiratory droplets produced by sneeze or cough during prodromal period  or direct contact with nasal or throat secretions from an infected person,  which continues up to few days after rash appears.
  • Less commonly, it is spread by airborne aerosolised droplet nuclei or by indirect contact with freshly contaminated articles.
  • More serious outcomes in malnurished children, people with deficient cell mediated immunity.


  • Measles virus invades the cells lining the upper respiratory tracts i.e respiratory epithelium of the nasopharynx and spreads to the regional lymph nodes
  • After 2-3 days of replication in these sites, a primary viraemia widens the infection to the reticuloendothelial system where further replication takes place.
  • Secondary viraemia occurs and the virus enters skin, conjunctivae, respiratory tract and other organs, including the spleen, thymus, lung, liver, and kidney and further replication occurs.
  • Appearances of rash: (because of cytotoxic T cells attacks measles virus infected vascular endothelial cells in the skin).
  • Formation of Multinucleated giant cells.

Clinical features of Measles

  • Incubation period: 10-14 days
  • Prodromal phase: Characterized by fever, conjunctivitis (causing photophobia), running nose, and coughing
 Fig: Clinical features of typical measles - time course from onset of illness
Fig: Clinical features of typical measles – time course from onset of illness
  • Appearance of Koplik’s spot (bright red lesions with the white, central dot) # Diagnostic feature
Koplik's Spot
Koplik’s Spot
  • Appearance  of Maculopapular rashes, common features of which includes:
    Child infected with Measles  Source:: CDC
    Child infected with Measles
    Source:: CDC
    • Occurs 5‐7 days after symptoms    
    • Lasts 3 or more days
    • Brownish hue
    • Progresses from face to body to extremities
    • Rash becomes confluent as it progresses
    • Rash affects palms and soles
    • Soon after the rash appears, the patient is no longer infectious.

Complications  because of Measles infections

  • Encephalitis: 1 per 1000 cases
  • Subacute sclerosing panencephalitis (SSPE): Fatal disease of nervous system can develop after several years after measles.
  • Giant cell pneumonia
  • Co-infections:

–     Secondary bacterial pneumonia –     Bacterial otitis media

  • Increased risk of still birth in pregnant women infected with measles.
  • Measles virus infection of fetus causes fetal death
  • Atypical measles develops in some people who were given killed vaccine and subsequently infected with measles virus.

Laboratory diagnosis of measles

  • Most diagnoses are made on clinical grounds; presence of koplik’s spot provides a definitive diagnosis.
  • If laboratory diagnosis is necessary, it can be done by
  • Isolation of virus in a cell culture
  • a positive serologic test for measles IgM
  • Demonstrating rise in antiviral antibody titer of greater than four-fold.
  • Identification of measles virus RNA from a clinical specimen by PCR


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