Oct 11, 2012.rtf

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Department
Molecular Genetics and Microbiology
Course
MGY440H1
Professor
Richard Brown
Semester
Fall

Description
October 11, 2012 PAPERS FOR TODAY: S Guest et al J Virol 78 2004 M Ida-Husonuma et al J Virol 2005 79 T. Yoshikawa et al J Virol 80 4313-3425 Kuss et al 2008 4:6 - STUDENT PRESENTATION Lancaster et al. 2010 6:3 Kauder and Racaniello 2004 - J Clin Investigation 113 1743-1753 **** POLIOVIRUS - still endemic in Afghanistan, Pakistan, Nigeria; India has been polio-free for a year - these are wild-type cases of polio - not vaccine-associated cases - www.polioeradication.org - still an issue in parts of the world - polio the disease = paralysis - this would be caused by replication in upper spinal cord - virus is lytic - replicates, kills the neurons - if too many killed off, disease caused - fecal-oral - needs to cross intestinal epithelial, into bloodstream, and cross blood-brain barrier (endothelial barrier) to get into central nervous system - less than 1% develop paralysis - vaccines came out in the 1950s 1. Salk - inactivated virus injected - inducing antibody formation against viral proteins - antibodies neutralize virus in blood where they circulate - virus would have had to grow in intestinal tissue first, then get to bloodstream where neutralized by antibody - the Salk vaccine gives you the infection, but prevents the pathogenesis - neutralizes the virus on its way from intestine to brain, preventing the virus from reachin the brain and spinal cord - DOES NOT PREVENT INFECTION 2. Sabin - live attenuated virus - virus passaged through cell culture and animals MANY times so acquired mutations so can replicate but does not cause disease - reversion to original type is still an issue with these many passages - mutation within n
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