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Chapter 37 : Measles Virus

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Abstract:

Measles is one of the most important infectious diseases of humans and has caused millions of deaths since its emergence thousands of years ago. Measles virus (MV) is one of the most highly contagious infectious pathogens, and measles outbreaks can occur in populations in which fewer than 10% of persons are susceptible. Infection of the endothelial cells of small vessels in the lamina propria and dermis during the secondary viremia precedes infection of the overlying epithelium, and inflammatory changes in and around these vessels are an integral part of the local pathology and characteristic rash. MV-specific immune responses are essential for recovery from measles and for the establishment of long-term immunity to disease, but they also play a role in the pathogenesis of measles and its complications. Acute postinfectious measles encephalomyelitis is the most common neurologic complication of measles. A second form of measles encephalitis, subacute sclerosing panencephalitis (SSPE), is a rare delayed complication of measles that occurs in approximately 1 in 10,000 cases. The third form of measles encephalitis, measles inclusion body encephalitis (MIBE), is a progressive, generally fatal MV infection of the brain that occurs in immunocompromised patients. Different goals for measles control have been established, necessitating different vaccination strategies. Three broad goals can be defined: mortality reduction, regional elimination, and global eradication. Vitamin A is effective for the treatment of measles, and its administration has resulted in marked reductions in morbidity and mortality in hospitalized children with measles.

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37

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Figures

Image of FIGURE 1
FIGURE 1

MV growing in cell culture. An extracellular virion (large solid arrow) is coated with glycoprotein spikes (small open arrows), with the viral nucleocapsid (small solid arrows) positioned beneath the envelope. An infected cell has a region on the membrane (large open arrow) with viral glycoprotein spikes and subjacent viral nucleocapsids that is a site of MV maturation and budding. Free paramyxovirus nucleocapsids (small solid arrows) from a disrupted viron are shown in the inset. (Courtesy of Cynthia Goldsmith, William Bellini, and Erskine Palmer of the Centers for Disease Control and Prevention, Atlanta, GA.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 2
FIGURE 2

MV structure, genome, and replication cycle. (a) MV is a spherical, nonsegmented, single-stranded, negative-sense RNA virus. Of the six structural proteins, the phosphoprotein P, large protein L, and nucleoprotein N form the nucleocapsid that encloses the viral RNA. The hemagglutinin protein H, fusion protein F, and matrix protein M, together with lipids from the host cell membrane, form the viral envelope. (b) The MV RNA genome is composed of approximately 16,000 nucleotides encoding eight proteins, two of which (V and C) are nonstructural proteins alternatively translated from the P gene. (c) The H protein interacts with F to mediate attachment and fusion of the viral envelope with the host cell membrane through specific receptors (CD46 and CD150), enabling viral entry into the cell. The remaining MV proteins are involved in viral replication. The P protein regulates transcription, replication, and assembly of nucleocapsids. The M protein is critical for viral assembly. (From reference with permission of the publisher.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 3
FIGURE 3

Basic pathogenesis of MV infection. Panels summarize features of the pathogenesis of MV infection. (Top) Spread of the virus from the initial site of infection in the respiratory epithelia to the skin. Sites of infection are overlaid with virus titer. (Middle) Appearance of clinical signs and symptoms in relation to viral replication and the immune responses. (Bottom) Immune responses to measles virus. The clinical manifestations arise coincident with the onset of the immune response. (From reference with permission of the publisher.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 4
FIGURE 4

Histopathology of Koplik’s spots (A) and the skin rash (B) of measles. The epidermal changes in both are characterized by multinucleated giant cells (arrows), focal parakeratosis, dyskeratosis and spongiosis, intracellular edema, and a sparse lymphocytic infiltrate. (Courtesy of D. W. R. Suringa, Tampa, FL.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 5
FIGURE 5

Potential mechanisms of immune suppression following MV infection. (From reference with permission of the publisher.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 6
FIGURE 6

Schematic diagram of the clinical course of a typical case of measles. (From reference with permission of Elsevier.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 7
FIGURE 7

Measles rash. Note the characteristic blotchy appearance. (From reference with permission of the publisher.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 8
FIGURE 8

Measles giant-cell pneumonia. Two multinucleated epithelial giant cells are visible in alveolar spaces in the lung of an immunosuppressed child who died of giant cell pneumonia. Eosinophilic Cowdry type A inclusion bodies are visible in many nuclei (arrows). (From reference with permission of the Massachusetts Medical Society.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Image of FIGURE 9
FIGURE 9

Measles vaccines. Most attenuated measles vaccines were developed from the Edmonston strain of MV. The Edmonston B vaccine was the first licensed measles vaccine but was associated with a high frequency of fever and rash. The further attenuated Schwarz and Edmonston-Zagreb vaccines are widely used throughout the world. The Moraten vaccine is the only measles vaccine used in the United States. (From reference with permission of the publisher.)

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
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Tables

Generic image for table
TABLE 1

Major structural and regulatory proteins of MV

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37
Generic image for table
TABLE 2

Neurologic complications of measles

Citation: Moss W, Griffin D. 2009. Measles Virus, p 849-875. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch37

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