Measles Virus


Measles virus (MV) is responsible for a childhood infection characterised by a maculopapular rash, dry cough, coryza, conjunctivitis and photophobia. Although mild in developed countries, the infection is associated with significant morbidity in developing countries and still kills more than 200 000 children per annum even though it is a vaccine preventable disease. The virus replication cycle is well understood and the molecular description of the virus has progressed to a stage where the main emphasis of research has reverted towards understanding the pathogenesis and molecular basis of virus attenuation. Such knowledge will assist in the development of new vaccines and serve to increase our understanding of epidemiology and transmission. Our ability to make recombinant viruses that express autofluorescent proteins from additional transcription units within the genome has created a paradigm shift in changing our view of MV from simply a ’respiratory infection‘ causing agent to one that affects the immune system in a serious and potentially dangerous manner. Identification of the early target cells as alveolar macrophages and/or dendritic cells in the deep lung alongside understanding the early events in viral pathogenesis helps shed light on how this highly infectious agent establishes such a profoundly immunosuppressive disease in the host.

Key Concepts:

  • Measles is a relatively simple enveloped, negative‐sensed RNA virus which contains only six genes.

  • Measles virus is a highly infectious agent, which causes a profound immunosuppression and a severe disease in susceptible individuals.

  • The molecular basis of the immunosuppression is unknown.

  • A highly efficacious vaccine has been developed, although the molecular basis of the attenuation remains an enigma.

  • It is essential to vaccinate 95% of the birth cohort as the virus is so infectious and when vaccine uptake levels decrease in disease‐free regions importations from endemic parts of the world often occur.

  • The vaccine is exceptionally thermolabile and this is challenging for those involved in delivering the product to remote areas of the developing world and in areas where conflict is rife.

  • Recombinant measles viruses have helped to define the early steps in the establishment of an infection.

  • Measles has been considered for eradication although the potential for cross‐species infection is being considered due to the cross‐protective morbillivirus antibodies which are elicited.

Keywords: measles virus; paramyxovirus; nonsegmented negative‐strand RNA virus; genome; measles; subacute sclerosing panencephalitis

Figure 1.

The arrangement of genes of the measles virus genome. Information concerning the nucleotides in each gene are given in Table . Genes are not to scale.

Figure 2.

Electron micrographs showing the formation of Y forms as intermediates in the intracellular replication of the ribonucleocapsids of measles virus. Magnification factor ×100 000. Courtesy of Dr Dermott SE, The Queen's University of Belfast.



Anonymous (2004) Progress toward measles elimination – region of the Americas, 2002–2003. Annals of Pharmacotherapy 38: 1108.

Avota E, Gassert E and Schneider‐Schaulies S (2010) Measles virus‐induced immunosuppression: from effectors to mechanisms. Medical Microbiology and Immunology 199: 227–237.

Bellini WJ, Englund G, Rozenblatt S, Arnheiter H and Richardson CD (1985) Measles virus P gene codes for two proteins. Journal of Virology 53: 908–919.

Bhella D, Ralph A, Murphy LB and Yeo RP (2002) Significant differences in nucleocapsid morphology within the Paramyxoviridae. Journal of General Virology 83: 1831–1839.

Buynak EB, Weibel RE, Mclean AA and Hilleman MK (1976) Long‐term persistence of antibody following Enders’ original and More attenuated live measles virus vaccine. Proceedings of the Society for Experimental Biology and Medicine 153: 441–443.

Caignard G, Guerbois M, Labernardiere JL et al. (2007) Measles virus V protein blocks Jak1‐mediated phosphorylation of STAT1 to escape IFN‐alpha/beta signaling. Virology 368: 351–362.

Calain P and Roux L (1993) The rule of six, a basic feature for efficient replication of Sendai virus defective interfering RNA. Journal of Virology 67: 4822–4830.

Cathomen T, Mrkic B, Spehner D et al. (1998) A matrix‐less measles virus is infectious and elicits extensive cell fusion: consequences for propagation in the brain. EMBO Journal 17: 3899–3908.

Cattaneo R, Kaelin K, Baczko K and Billeter MA (1989a) Measles virus editing provides an additional cysteine‐rich protein. Cell 56: 759–764.

Cattaneo R, Rebmann G, Baczko K, ter Meulen V and Billeter MA (1987) Altered ratios of measles virus transcripts in diseased human brains. Virology 160: 523–526.

Cattaneo R, Schmid A, Spielhofer P et al. (1989b) Mutated and hypermutated genes of persistent measles viruses which caused lethal human brain diseases. Virology 173: 415–425.

Erlenhöfer C, Duprex WP, Rima BK, ter Meulen V and Schneider‐Schaulies J (2002) Analysis of receptor (CD46, CD150) usage by measles virus. Journal of General Virology 83: 1431–1436.

Grenfell BT, Bjornstad ON and Kappey J (2001) Travelling waves and spatial hierarchies in measles epidemics. Nature 414: 716–723.

Griffin DE (1991) Immunologic abnormalities accompanying acute and chronic viral infections. Reviews of Infectious Diseases 13(suppl. 1): S129–S133.

Griffin DE (2010) Measles virus‐induced suppression of immune responses. Immunological Reviews 236: 176–189.

Griffin DE, Ward BJ, Jauregui E, Johnson RT and Vaisberg A (1989) Immune activation in measles. New England Journal of Medicine 320: 1667–1672.

Hashiguchi T, Ose T, Kubota M et al. (2011) Structure of the measles virus hemagglutinin bound to its cellular receptor SLAM. Nature Structural & Molecular Biology 18: 135–141.

Hausmann S, Garcin D, Delenda C and Kolakofsky D (1999) The versatility of paramyxovirus RNA polymerase stuttering. Journal of Virology 73: 5568–5576.

Lamb RA (1993) Paramyxovirus fusion: a hypothesis for changes. Virology 197: 1–11.

Lamb RA and Kolakofsky D (2001) Paramyxoviridae: the viruses and their replication In: Knipe DM and Howley PM (eds) Fields Virology, pp. 1305–1340. Philadelphia: Lippincott Williams & Wilkins.

Leonard VH, Sinn PL, Hodge G et al. (2008) Measles virus blind to its epithelial cell receptor remains virulent in rhesus monkeys but cannot cross the airway epithelium and is not shed. Journal of Clinical Investigation 118: 2448–2458.

Liston P and Briedis DJ (1994) Measles virus V protein binds zinc. Virology 198: 399–404.

Low N, Kraemer S, Schneider M and Restrepo AM (2008) Immunogenicity and safety of aerosolized measles vaccine: systematic review and meta‐analysis. Vaccine 26: 383–398.

Melnick JL (1996) Thermostability of poliovirus and measles vaccines. Developments in Biological Standardization 87: 155–160.

Naniche D, Varior‐Krishnan G, Cervoni F et al. (1993) Human membrane cofactor protein (CD46) acts as a cellular receptor for measles virus. Journal of Virology 67: 6025–6032.

Navaratnarajah CK, Oezguen N, Rupp L et al. (2011) The heads of the measles virus attachment protein move to transmit the fusion‐triggering signal. Nature Structural & Molecular Biology 18: 128–134.

Nozawa Y, Ono N, Abe M, Sakuma H and Wakasa H (1994) An immunohistochemical study of Warthin‐Finkeldey cells in measles. Pathology International 44: 442–447.

Patterson JB, Thomas D, Lewicki H, Billeter MA and Oldstone MB (2000) V and C proteins of measles virus function as virulence factors in vivo. Virology 267: 80–89.

Retief F and Cilliers L (2010) Measles in antiquity and the Middle Ages. South African Medical Journal 100: 216–217.

Rima BK, Collin AMJ and Earle JAP (2003) Completion of the sequence of a cetacean morbillivirus and comparative analysis of the complete genome sequences of four morbilliviruses. Virus Genes 30(1): 113–119.

Rima BK and Duprex WP (2005) Molecular mechanisms of measles virus persistence. Virus Research 111: 132–147.

Rima BK and Duprex WP (2006) Morbilliviruses and human disease. Journal of Pathology 208: 199–214.

Rima BK and Duprex WP (2009) The measles virus replication cycle. Current Topics in Microbiology and Immunology 329: 77–102.

Rima BK, Earle JA, Baczko K, Rota PA and Bellini WJ (1995) Measles virus strain variations. Current Topics in Microbiology and Immunology 191: 65–83.

Rota JS, Rota PA, Redd SB et al. (1998) Genetic analysis of measles viruses isolated in the United States, 1995–1996. Journal of Infectious Diseases 177: 204–208.

Rota JS, Wang ZD, Rota PA and Bellini WJ (1994) Comparison of sequences of the H, F, and N coding genes of measles virus vaccine strains. Virus Research 31: 317–330.

Rozenblatt S, Koch T, Pinhasi O and Bratosin S (1979) Infective substructures of measles virus from acutely and persistently infected cells. Journal of Virology 32: 329–333.

Schneider‐Schaulies J, ter Meulen V and Schneider‐Schaulies S (2003) Measles infection of the central nervous system. Journal of Neurovirology 9: 247–252.

Shaffer JA, Bellini WJ and Rota PA (2003) The C protein of measles virus inhibits the type I interferon response. Virology 315: 389–397.

de Swart RL, Ludlow M, de Witte L et al. (2007) Predominant infection of CD150+ lymphocytes and dendritic cells during measles virus infection of macaques. PLoS Pathogen 3: e178.

Tahara M, Takeda M, Shirogane Y et al. (2008) Measles virus infects both polarized epithelial and immune cells by using distinctive receptor‐binding sites on its hemagglutinin. Journal of Virology 82: 4630–4637.

Tatsuo H, Ono N, Tanaka K and Yanagi Y (2000) SLAM (CDw150) is a cellular receptor for measles virus. Nature 406: 893–897.

Taylor MJ, Godfrey E, Baczko K et al. (1991) Identification of several different lineages of measles virus. Journal of General Virology 72(part 1): 83–88.

Thorne HV and Dermott E (1977) Y‐forms as possible intermediates in the replication of measles virus nucleocapsids. Nature 268: 345–347.

Vincent S, Gerlier D and Manie SN (2000) Measles virus assembly within membrane rafts. Journal of Virology 74: 9911–9915.

Vongpunsawad S, Oezgun N, Braun W and Cattaneo R (2004) Selectively receptor‐blind measles viruses: identification of residues necessary for. Journal of Virology 78: 302–313.

de Vries RD, Lemon K, Ludlow M et al. (2010) In vivo tropism of attenuated and pathogenic measles virus expressing green fluorescent protein in macaques. Journal of Virology 84: 4714–4724.

Watanabe M, Hirano A, Stenglein S et al. (1995) Engineered serine protease inhibitor prevents furin‐catalyzed activation of the fusion glycoprotein and production of infectious measles virus. Journal of Virology 69: 3206–3210.

Yanagi Y, Takeda M, Ohno S and Hashiguchi T (2009) Measles virus receptors. Current Topics in Microbiology and Immunology 329: 13–30.

Zhu J, Ding Y, Gao F et al. (2003) Crystallization and preliminary X‐ray crystallographic analysis of the trimer core from measles virus fusion protein. Acta Crystallographica Section D Biological Crystallography 59: 587–590.

Further Reading

Billeter MA and ter Meulen V (eds) (1995) Measles virus. Current Topics in Microbiology and Immunology 191: 1–196.

Griffin DE (2007) Measles virus. In: Knipe DM and Howley PM (eds) Fields Virology, 5th edn, pp. 1551–1585. Philadelphia, PA: Lippincott, Williams & Wilkins.

Griffin DE and Oldstone MB (eds) (2009) Measles. History and basic biology. Current Topics in Microbiology and Immunology. 329: 1–191.

Perry PT and Halsey NA (2004) The clinical significance of measles: a review. Journal of Infectious Diseases 189: S4–S16.

Rota PA and Bellini WJ (2003) Update on the global distribution of genotypes of wild type measles viruses. Journal of Infectious Diseases 187: S270–S276.

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Rima, Bertus K, and Duprex, W Paul(Jul 2011) Measles Virus. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000418.pub3]