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Measles

Pathogenesis

Gary S. Marshall, MD 
Reviewed on October 18, 2024
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Infection Pathway

The first host cells to be infected by measles morbillivirus (MeV) are epithelial cells and intraepithelial immune cells (primarily macrophages and dendritic cells) in the respiratory tract. From there, the virus is readily transmitted to neighboring lymphoid tissues, infecting thymocytes, T and B lymphocytes and hematopoietic stem cells. Infected lymphocytes then mediate the systemic spread of the virus, infecting immune, epithelial and endothelial cells in non-lymphoid tissues and organs throughout the body, while the total virus titer increases (Figure 1-3). Clinical symptoms are generally absent during the initial spread phase, but once the virus reaches the peripheral lymphoid organs, prodromal symptoms – fever and one or more of cough, coryza, or conjunctivitis – appear as a direct consequence of viral replication-induced epithelial cell damage.

The maculopapular exanthema (eruptive rash) that characterizes measles in immunocompetent hosts occurs as a…

Infection Pathway

The first host cells to be infected by measles morbillivirus (MeV) are epithelial cells and intraepithelial immune cells (primarily macrophages and dendritic cells) in the respiratory tract. From there, the virus is readily transmitted to neighboring lymphoid tissues, infecting thymocytes, T and B lymphocytes and hematopoietic stem cells. Infected lymphocytes then mediate the systemic spread of the virus, infecting immune, epithelial and endothelial cells in non-lymphoid tissues and organs throughout the body, while the total virus titer increases (Figure 1-3). Clinical symptoms are generally absent during the initial spread phase, but once the virus reaches the peripheral lymphoid organs, prodromal symptoms – fever and one or more of cough, coryza, or conjunctivitis – appear as a direct consequence of viral replication-induced epithelial cell damage.

The maculopapular exanthema (eruptive rash) that characterizes measles in immunocompetent hosts occurs as a consequence of the adaptive immune response to the disseminated MeV and signals the beginning of viral clearance. By the time the rash subsides, infectious virions have typically been fully cleared, although viral RNA may be detectable in the blood for a number of weeks thereafter (Figure 1-4).

The adaptive immune response to MeV infection is also responsible for hyperemia and edema, while keratoconjunctivitis occurs due to infection of keratinocytes. Complications of measles, including pneumonia and otitis media, are typically not caused by viral replication or clearance, but rather secondary bacterial infections.

Enlarge  Figure 1-3: Systemic Spread of MeV. Plaque-forming unit (PFU). Source: Adapted from: Rainwater-Lovett K, Moss WJ. Measles (Rubeola). In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. <em>Harrison's Principles of Internal Medicine, 20e</em>. McGraw-Hill Education; 2018. Originally from: Moss WJ, et al. <em>Nat Rev Microbiol</em>. 2006 Dec;4(12):900-8.
Figure 1-3: Systemic Spread of MeV. Plaque-forming unit (PFU). Source: Adapted from: Rainwater-Lovett K, Moss WJ. Measles (Rubeola). In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 20e. McGraw-Hill Education; 2018. Originally from: Moss WJ, et al. Nat Rev Microbiol. 2006 Dec;4(12):900-8.
Enlarge  Figure 1-4: Measles Rash and Viral Clearance. Infectious virions are shown in blue, rash in red and viral RNA (detectable in blood) as the dotted line. Source: Adapted from: Griffin DE, et al. <em>FEMS Microbiol Rev</em>. 2012 May;36(3):649-62.
Figure 1-4: Measles Rash and Viral Clearance. Infectious virions are shown in blue, rash in red and viral RNA (detectable in blood) as the dotted line. Source: Adapted from: Griffin DE, et al. FEMS Microbiol Rev. 2012 May;36(3):649-62.

References

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