Abstract
GENERAL COMMENTARY article Front. Microbiol., 24 December 2012Sec. Virology Volume 3 - 2012 | https://doi.org/10.3389/fmicb.2012.00431
Highlights
In the last 25 years, no less than 10 dramatic morbilliviral epidemics have occurred among free-ranging pinniped and cetacean species and populations worldwide
Nectin-4—a cell adhesion molecule—has been recently identified as an additional receptor selectively binding Measles Virus (MeV) H antigen, thereby allowing viral entry into host’s epithelial cells (Sato et al, 2012). Enough, both SLAM and nectin-4 are not expressed by neuronal and endothelial cells (Sato et al, 2012), whereas morbilliviruses—which are known to be carried by SLAM+ immune cells into the bloodstream (Sato et al, 2012)—necessarily need to cross the blood-brain barrier before invading the host’s cerebral parenchyma with its resident neuron cell populations
How does the virus achieve these “ambitious” goals and, not less importantly, how does it persist “undisturbed” inside the host’s brain, progressively giving rise to human Sclerosing Panencephalitis” (SSPE) (Rima and Duprex, 2006), canine Old Dog Encephalitis” (ODE) (Rima et al, 1987), and their “disease analogue” in wild dolphins (Di Guardo et al, 2011a, 2012; Soto et al, 2011)? One possible answer to the above questions could reside in a “selectively/exclusively neurotropic behavior” of given morbilliviral strains inside their hosts, with a crucial determinant of such a behavior being likely represented by the specific interaction of the virus with a receptor molecule selectively and/or consistently expressed by neurons
Summary
In the last 25 years, no less than 10 dramatic morbilliviral epidemics have occurred among free-ranging pinniped and cetacean species and populations worldwide. These DMV-infected cetaceans showed immunohistochemical and/or biomolecular evidence of morbilliviral antigen and/or genome exclusively in their brain tissue (Di Guardo et al, 2011a, 2012; Soto et al, 2011), to what reported in SSPE-affected patients (Rima and Duprex, 2006) and ODE-affected dogs (Rima et al, 1987).
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