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Appendix G: Influenza A and SARS-CoV
Pages 161-162

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From page 161...
... The effects of restoring a full length functional PB1-F2 protein on 2009 swine H1N1 in vivo pathogenesis are difficult to predict because its virulence-enhancing activities may depend on co-evolutionary changes elsewhere in the genome. As a working model for predicting virulence from sequence information, the preponderance of influenza data suggest that restoration of a full length PB1-F2 protein will enhance the virulence of swine H1N1 -- a hypothesis that will probably be tested using reverse genetics in the near future (McAuley, Zhang et al.)
From page 162...
... On the basis of sequence, it was not possible to pre dict that the two highly divergent coronavirus RBDs would engage a similar "hot spot" on the surface of the ACE2 receptor and thus mediate docking and entry into cells. Moreover, the pathogenic potential of the two human coronaviruses are distinct: SARS-CoV causes an atypical pneumonia that results in acute respiratory distress syndrome with mortality exceeding 50 percent in people over 60 years old, whereas NL63-CoV causes a self-limiting denuding bronchiolitis and croup, primarily in infants and children.


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