Current Animal Models: Transgenic Animal Models for the Study of Measles Pathogenesis
Animal models are highly important to understand the pathologic mechanisms of viral diseases. Therefore, the lack of a suitable animal model has greatly hindered the research into the pathogenesis of measles. Identification of two human receptors for measles virus, CD46 and CD150 (SLAM) has opened new perspectives in this field. During the last decade, numerous transgenic animal models have been developed in order to humanize mice and use them to study measles infection and virus—host interactions. Despite their limitations, these models have provided remarkable insights in different aspects of measles infection, providing a better understanding of virus-induced neuropathology, immunosuppression, mechanisms of virus virulence, and contribution of innate and adaptive immune response in viral clearance. They should certainly continue to help in studies of the host and viral factors that are important in measles infection and in developing of new antiviral agentsand measles virus-based vaccines. In addition, as CD46 serves as a receptor for two other human viruses, some of these models may also find an important application in the study of adenovirus and herpesvirus 6 infection. In this review, we describe different CD46 and CD150 transgenic models and detail their utilization in the study of various aspects of measles pathogenesis.
KeywordsWest Nile Virus Measle Virus Membrane Cofactor Protein Measle Virus Infection Signaling Lymphocytic Activation Molecule
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- Lorin C, Mollet L, Delebecque F, Combredet C, Hurtrel B, Charneau P, Brahic M, Tangy F (2004)A single injection of recombinant measles virus vaccines expressing human immunodeficiency virus (HIV) type 1 clade B envelope glycoproteins induces neutralizing antibodies and cellular immune responses to HIV. J Virol 78:146–157PubMedCrossRefGoogle Scholar
- Patterson JB, Cornu TI, Redwine J, Dales S, Lewicki H, Holz A, Thomas D, Billeter MA,Oldstone MB (2001) Evidence that the hypermutated M protein of a subacute sclerosing pan-encephalitis measles virus actively contributes to the chronic progressive CNS disease.Virology 291:215–225PubMedCrossRefGoogle Scholar
- Shingai M, Inoue N, Okuno T, Okabe M, Akazawa T, Miyamoto Y, Ayata M, Honda K, Kurita-Taniguchi M, Matsumoto M et al (2005) Wild-type measles virus infection in human CD46/CD150-transgenic mice: CD11c-positive dendritic cells establish systemic viral infection. J Immunol 175:3252–3261PubMedGoogle Scholar
- Thorley BR, Milland J, Christiansen D, Lanteri MB, McInnes B, Moeller I, Rivailler P, Horvat B,Rabourdin-Combe C, Gerlier D et al (1997) Transgenic expression of a CD46 (membrane cofactor protein) minigene: studies of xenotransplantation and measles virus infection. Eur J Immunol 27:726–734PubMedCrossRefGoogle Scholar
- Tishon A, Lewicki H, Andaya A, McGavern D, Martin L, Oldstone MB (2006) CD4 T cell control primary measles virus infection of the CNS: regulation is dependent on combined activity with either CD8 T cells or with B cells: CD4 CD8 or B cells alone are ineffective. Virology 347:234–245PubMedCrossRefGoogle Scholar
- WHO (2002) Scaling up the response to infectious diseases.www.who.int/infectious-disease-report/2002/introduction.html. Cited 26 May 2008