The pathogenesis of measles

Department of Virology, Erasmus MC, PO Box 2040, 3000 CA, Rotterdam, The Netherlands.
Current opinion in virology 04/2012; 2(3):248-55. DOI: 10.1016/j.coviro.2012.03.005
Source: PubMed


Measles is an important cause of childhood morbidity and mortality in developing countries. Measles virus (MV) is transmitted via the respiratory route and causes systemic disease. Over the last decade, identification of new cellular receptors and studies in animal models have challenged the historic concepts of measles pathogenesis. It is thought that MV enters the host by infection of alveolar macrophages and/or dendritic cells in the airways, and is amplified in local lymphoid tissues. Viremia mediated by infected CD150+ lymphocytes results in systemic dissemination. Infection of lymphocytes and dendritic cells in the respiratory submucosa facilitates basolateral infection of epithelial cells via the newly identified receptor Nectin-4. Concomitant and extensive epithelial damage may contribute to efficient transmission to the next host.

18 Reads
  • Source
    • "blood monocytes from clinically healthy, FCoVinfected cats) would not be easy, but it would be very illuminating. The idea that a virus has to undergo sequential mutation in vivo in order to cause a specific disease is not unique to FIP (see, for example, the review on measles virus pathogenesis by de Vries et al., 2012), but we suggest it deserves closer attention in a number of veterinary and human diseases. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Feline coronavirus (FCoV) infections are endemic amongst cats worldwide. The majority of infections are asymptomatic, or result only in mild enteric disease. However, approximately 5% of cases develop feline infectious peritonitis (FIP), a systemic disease that is a frequent cause of death in young cats. In this study, we report the complete coding genome sequences of six FCoVs; three from fecal samples from healthy cats and three from tissue lesion samples from cats with confirmed FIP. The six samples were obtained over a period of eight weeks at a single-site cat rescue and rehoming center in the UK. We found amino acid differences are located at 44 positions across an alignment of the six virus translatomes and, at 21 of these positions, the differences fully or partially discriminate between the genomes derived from the fecal samples and the genomes derived from tissue lesion samples. In this study, two amino acid differences fully discriminate the two classes of genomes; these are both located in the S2 domain of the virus surface glycoprotein gene. We also identified deletions in the 3c protein ORF of genomes from two of the FIP samples. Our results support previous studies that implicate S protein mutations in the pathogenesis of FIP.
    Journal of General Virology 02/2015; 96(Pt_6). DOI:10.1099/vir.0.000084 · 3.18 Impact Factor
  • Source
    • "This suggests that the alveolar macrophages may play a significant role in the pathogenesis associated with PPRV infection, although this may depend on the route of infection. In recent studies with aerosol infection of measles virus, it has been shown that the virus enters the host by infection of alveolar macrophages and/or dendritic cells in the airways, and is amplified in local lymphoid tissues [34]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Peste des petits ruminants (PPR) is a viral disease which primarily affects small ruminants, causing significant economic losses for the livestock industry in developing countries. It is endemic in Saharan and sub-Saharan Africa, the Middle East and the Indian sub-continent. The primary hosts for peste des petits ruminants virus (PPRV) are goats and sheep; however recent models studying the pathology, disease progression and viremia of PPRV have focused primarily on goat models. This study evaluates the tissue tropism and pathogenesis of PPR following experimental infection of sheep and goats using a quantitative time-course study. Upon infection with a virulent strain of PPRV, both sheep and goats developed clinical signs and lesions typical of PPR, although sheep displayed milder clinical disease compared to goats. Tissue tropism of PPRV was evaluated by real-time RT-PCR and immunohistochemistry. Lymph nodes, lymphoid tissue and digestive tract organs were the predominant sites of virus replication. The results presented in this study provide models for the comparative evaluation of PPRV pathogenesis and tissue tropism in both sheep and goats. These models are suitable for the establishment of experimental parameters necessary for the evaluation of vaccines, as well as further studies into PPRV-host interactions.
    PLoS ONE 01/2014; 9(1):e87145. DOI:10.1371/journal.pone.0087145 · 3.23 Impact Factor
  • Source

    Proceedings of the National Academy of Sciences 08/2012; 109(37):14724-5. DOI:10.1073/pnas.1212243109 · 9.67 Impact Factor
Show more