-HA binding preferences of influenza viruses of H1 and H3 subtypes in humans are on a2-6-sialylated glycans on the epithelial lining of the lower and upper respiratory system.
-Once virus is attached to the appropriate a2-6-sialylated receptor in host cell, a slightly acidic environment contributes the fusion between the endosome and the viral envelop which then assist in delivering the viral RNA to cell’s nucleus and triggering viral replication, thus reproducing and damaging the host cell as it leaves the membrane (Rapid, 2012).
-Cleavage is essential for viral infectivity and the enzyme necessary for cleavage is a trypsin-like protease which is believed to be released from Clara cells in the epithelial lining of the respiratory tract;this enzyme is limited in other organs, human influenza viruses normally do not spread beyond the respiratory tract (Rapid, 2012)
-Low pathogenicity HAs are similar to the one in human and only have one binding site thus restricting the spread of viruses; on the other hand the high-pathogenicity HAs have multi-basic cleavage sites that rely on a intracellular furin-like enzyme, that happen to be available in all cells, for cleavage, which causes avian influenza to spread throughout the body and causing death (Rapid, 2012)
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-High-pathogenicity multi-based cleavage sites could be the determinant of the spread of human viral
pathogenicity; for example, the extremely pathogenic Spanish flu does not have
a multi-base cleavage binding site, whereas the highly pathogenic H5N1 avian influenza virus does, thus making a
high-rated fatal influenza virus
(Rapid, 2012).
-Research by Guan et al (2010) has strong evidence that pandemics of influenza viruses do not result from infection shortly before pandemic episode but rather are results of new subtypes or strains of viruses combining with remaining strains from previous pandemics that take years to develop. Since ferrets have similar respiratory lining and lung physiology as humans, a study by Pearce et al (2011) was helpful to determine that Calu-3 cells from the bronchial epithelial lining increase the pathogenicity and transmissibility of origin H3N2 influenza viruses thus suggesting that it has potential to hurt human beings. -Pandemic H1N1 viral characteristic are similar to the ones of seasonal influenza A viruses when it comes to viral shedding, clinical illness, and transmissibility except that it is more pathogenic in children due to the lack of preexisting immunity to pandemic influenza viruses. |