Abnormal Development - Measles Virus

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Child with Measles back rash day 3
Child with Measles back rash day 3 (CDC)
Measles virus
Measles virus (CDC)

Measles (rubeola, German Measles, Three-Day Measles) is a paramyxovirus appearing mainly as a respiratory viral infection, clinically different from rubella. A single-stranded RNA virus which is highly contagious. Before measles vaccination (USA 1963) more than 90% of children had an infection before puberty and in developing countries it is still a common and often fatal childhood disease. Childhood immunisation and immunity persists in only about 80% of adults.

Pregnancy effects of measles results in a higher risk of premature labor, spontaneous abortion, low-birth-weight, and possibly rare cases of birth defects with no definable pattern of malformation.[1]

20 March 2014 - Measles Elimination Achieved in Australia

The World Health Organization (WHO) announced that measles elimination had been achieved by Australia, Macao (China), Mongolia and the Republic of Korea.

Some Recent Findings

  • Rubella and congenital rubella syndrome control and elimination - global progress, 2000-2012[2] "Rubella virus usually causes a mild fever and rash in children and adults. However, infection during pregnancy, especially during the first trimester, can result in miscarriage, stillbirth, or infants with congenital malformations, known as congenital rubella syndrome (CRS). In 2011, the World Health Organization (WHO) updated guidance on the preferred strategy for introduction of rubella-containing vaccine (RCV) into national routine immunization schedules with an initial wide-age-range vaccination campaign that includes children aged 9 months-15 years. WHO also urged all member states to take the opportunity offered by accelerated measles control and elimination activities as a platform to introduce RCVs. The Global Measles and Rubella Strategic Plan (2012-2020) published by the Measles Rubella Initiative partners in 2012 and the Global Vaccine Action Plan endorsed by the World Health Assembly in 2012 include milestones to eliminate rubella and CRS in two WHO regions by 2015, and eliminate rubella in five WHO regions by 2020. This report summarizes the global progress of rubella and CRS control and elimination during 2000-2012. As of December 2012, a total of 132 (68%) WHO member states had introduced RCV, a 33% increase from 99 member states in 2000. A total of 94,030 rubella cases were reported to WHO in 2012 from 174 member states, an 86% decrease from the 670,894 cases reported in 2000 from 102 member states."
  • Prolonged persistence of measles virus RNA is characteristic of primary infection dynamics[3] "Measles virus (MeV) is the poster child for acute infection followed by lifelong immunity. However, recent work shows the presence of MeV RNA in multiple sites for up to 3 mo after infection in a proportion of infected children. Here, we use experimental infection of rhesus macaques to show that prolonged RNA presence is characteristic of primary infection. We found that viral RNA persisted in the blood, respiratory tract, or lymph nodes four to five times longer than the infectious virus and that the clearance of MeV RNA from blood happened in three phases: rapid decline coincident with clearance of infectious virus, a rebound phase with increases up to 10-fold, and a phase of slow decrease to undetectable levels. ... Based on the model, we demonstrate that viral dynamics, although initially regulated by T cells, require antibody to eliminate viral RNA. These results have profound consequences for our view of acute viral infections, the development of prolonged immunity, and, potentially, viral evolution."
  • Rapid titration of measles and other viruses: optimization with determination of replication cycle length[4] "Measles virus (MV) is a member of the Paramyxoviridae family and an important human pathogen causing strong immunosuppression in affected individuals and a considerable number of deaths worldwide. Currently, measles is a re-emerging disease in developed countries. MV is usually quantified in infectious units as determined by limiting dilution and counting of plaque forming unit either directly (PFU method) or indirectly from random distribution in microwells (TCID50 method). Both methods are time-consuming (up to several days), cumbersome and, in the case of the PFU assay, possibly operator dependent. ...Overall, performing the assay takes only 24-30 hours for MV strains, 12 hours for VSV, and 52 hours for HIV-1. The step-by-step procedure we have set up can be, in principle, applicable to accurately quantify any virus including lentiviral vectors, provided that a virus encoded gene product can be detected by flow cytometry."
  • Since January 2011 Romania has been experiencing a measles outbreak with 2,072 cases notified in 29 of the 42 Romanian districts.[5] "This report underlines once more the need for additional measures targeting susceptible populations to achieve high vaccination coverage with two doses of measles-mumps-rubella vaccine."
  • The measles virus replication cycle[6] "This review describes the two interrelated and interdependent processes of transcription and replication for measles virus. First, we concentrate on the ribonucleoprotein (RNP) complex, which contains the negative sense genomic template and in encapsidated in every virion. Second, we examine the viral proteins involved in these processes, placing particular emphasis on their structure, conserved sequence motifs, their interaction partners and the domains which mediate these associations."

Virus Structure

Identical genotype B3 sequences from measles patients in 4 countries
Identical genotype B3 sequences from measles patients in 4 countries, 2005.[7]

Lineage: Viruses; ssRNA viruses; ssRNA negative-strand viruses; Mononegavirales; Paramyxoviridae; Paramyxovirinae; Morbillivirus; Measles virus

  • ssRNA; linear; Length: 15,894 nt Measles virus, complete genome
  • virus replication involves a viral RNA-dependent RNA polymerase (vRdRp), using as a template a nucleocapsid (NC) made of a single strand of RNA in tight complex with the nucleoprotein (N).[8]
  • negative-strand genome contains six transcription units encoding the N, phospho (P), matrix (M), fusion (F), hemagglutinin (H), and large (L) or polymerase protein.
  • each N protein binds to 6 nucleotides.
  • the N polymer entirely covers the 15,894-nucleotide genome.
  • 23 known measles genotypes.

Model of cell virus RNA accumulation

The following 5 -step model has been described for cell virus accumulation following hours post-infection (hpi)[8]

  1. 0 to ~5 hpi - incoming viral RNA-dependent RNA polymerase (vRdRp) initiated primary transcription from every gene with no detectable lag phase.
  2. ~5 to ~12 hpi - mRNA accumulates exponentially.
  3. ~12 to ~24 hpi - mRNAs, genomes, and antigenomes accumulate exponentially because of the increase of both newly available template and vRdRp.
  4. ~24 to ~30 hpi - genomes and antigenomes continue to accumulate exponentially at the same rate, whereas the accumulation of the transcripts slows down.
  5. 30+ hpi - genome and antigenome accumulation slows down, and the cell content in viral transcripts tends to decrease.


Rubella and measles elimination in the Americas
Rubella and measles elimination in the Americas

Japan - first introduced to Japan in 1966 and adopted in the national regular immunization program from 1978.


  1. <pubmed>12850161</pubmed>
  2. Centers for Disease Control and Prevention (CDC). (2013). Rubella and congenital rubella syndrome control and elimination - global progress, 2000-2012. MMWR Morb. Mortal. Wkly. Rep. , 62, 983-6. PMID: 24304830
  3. Lin WH, Kouyos RD, Adams RJ, Grenfell BT & Griffin DE. (2012). Prolonged persistence of measles virus RNA is characteristic of primary infection dynamics. Proc. Natl. Acad. Sci. U.S.A. , 109, 14989-94. PMID: 22872860 DOI.
  4. Grigorov B, Rabilloud J, Lawrence P & Gerlier D. (2011). Rapid titration of measles and other viruses: optimization with determination of replication cycle length. PLoS ONE , 6, e24135. PMID: 21915289 DOI.
  5. Stanescu A, Janta D, Lupulescu E, Necula G, Lazar M, Molnar G & Pistol A. (2011). Ongoing measles outbreak in Romania, 2011. Euro Surveill. , 16, . PMID: 21871218
  6. Rima BK & Duprex WP. (2009). The measles virus replication cycle. Curr. Top. Microbiol. Immunol. , 329, 77-102. PMID: 19198563
  7. Rota J, Lowe L, Rota P, Bellini W, Redd S, Dayan G, van Binnendijk R, Hahné S, Tipples G, Macey J, Espinoza R, Posey D, Plummer A, Bateman J, Gudiño J, Cruz-Ramirez E, Lopez-Martinez I, Anaya-Lopez L, Holy Akwar T, Giffin S, Carrión V, de Filippis AM, Vicari A, Tan C, Wolf B, Wytovich K, Borus P, Mbugua F, Chege P, Kombich J, Akoua-Koffi C, Smit S, Bukenya H, Bwogi J, Baliraine FN, Kremer J, Muller C & Santibanez S. (2006). Identical genotype B3 sequences from measles patients in 4 countries, 2005. Emerging Infect. Dis. , 12, 1779-81. PMID: 17283637 DOI.
  8. 8.0 8.1 Plumet S, Duprex WP & Gerlier D. (2005). Dynamics of viral RNA synthesis during measles virus infection. J. Virol. , 79, 6900-8. PMID: 15890929 DOI.



Manikkavasagan G & Ramsay M. (2009). The rationale for the use of measles post-exposure prophylaxis in pregnant women: a review. J Obstet Gynaecol , 29, 572-5. PMID: 19757257 DOI.

Stein SJ & Greenspoon JS. (1991). Rubeola during pregnancy. Obstet Gynecol , 78, 925-9. PMID: 1923230

Enders M, Biber M & Exler S. (2007). [Measles, mumps and rubella virus infection in pregnancy. Possible adverse effects on pregnant women, pregnancy outcome and the fetus]. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz , 50, 1393-8. PMID: 17999132 DOI.

Ornoy A & Tenenbaum A. (2006). Pregnancy outcome following infections by coxsackie, echo, measles, mumps, hepatitis, polio and encephalitis viruses. Reprod. Toxicol. , 21, 446-57. PMID: 16480851 DOI.


Chiba ME, Saito M, Suzuki N, Honda Y & Yaegashi N. (2003). Measles infection in pregnancy. J. Infect. , 47, 40-4. PMID: 12850161

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Cite this page: Hill, M.A. (2024, April 14) Embryology Abnormal Development - Measles Virus. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Measles_Virus

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