What is the causative agent of measles?

Causative Agent of Measles

Measles is caused by measles virus (MeV), an enveloped RNA virus belonging to the genus Morbillivirus of the family Paramyxoviridae. 1, 2, 3

Viral Characteristics

• Measles virus is a single-stranded, negative-sense RNA virus with two major envelope glycoproteins: the hemagglutinin (H) protein and the fusion (F) protein 2, 3
• The H protein binds to cellular receptors—primarily signaling lymphocytic activation molecule family member 1 (SLAMF1, also called CD150) and nectin-4—to initiate viral entry 2, 3, 4
• The F protein mediates membrane fusion between the virus and host cell, or between infected cells and neighboring susceptible cells, allowing viral spread 2, 3

Transmission Mechanism

• The virus spreads through respiratory droplets and airborne transmission, making it one of the most contagious infectious agents known 1, 5, 6
• Patients are contagious from 4 days before rash onset to 4 days after rash appears 1, 5, 6
• The incubation period averages 10-12 days from exposure to prodrome and 14 days from exposure to rash (range: 7-18 days) 1, 5, 6

Primary Target Cells

• Dendritic cells and lymphocytes expressing CD150 (SLAMF1) are the primary target cells for initial measles virus infection 4
• Dendritic cells likely serve as the first cells infected in the respiratory tract, then traffic the virus to regional lymph nodes where they transmit it to lymphocytes 4
• During viremia, infected lymphocytes disseminate the virus throughout the body 4
• At late stages of infection, the virus also infects epithelial cells, despite these cells not expressing CD150, suggesting additional receptor mechanisms 4

Neuropathogenic Potential

• Measles virus can persist in the brain and cause subacute sclerosing panencephalitis (SSPE), a rare but fatal neurodegenerative disease that appears years after acute infection 1, 5, 2, 3
• SSPE-associated viral strains accumulate specific mutations in the F protein that enable the virus to use cell adhesion molecules (CADM1 and CADM2) as fusion-triggering molecules, facilitating spread between neurons 2, 3
• These hyperfusogenic mutations allow the virus to propagate in brain tissue that does not express the conventional receptors SLAMF1 and nectin-4 2, 3