Abstract
After intranasal inoculation of ferrets with influenza virus the upper respiratory tract infection diminishes during the second day and the onset of this reduction occurs earlier for an attenuated clone (64d) than for a virulent clone (7a) of the recombinant virus A/PR/8/34-A/England/939/69 (H3N2). The relevance of pyrexia and the nasal inflammatory response to this reduction in infection has been investigated.
Egg-grown Clone 64d was more thermobile than Clone 7a at normal and pyrexial temperatures when suspended in egg allantoic fluid or phosphate-buffered saline. However, in infected nasal washes, both clones were rapidly inactivated when the washes were incubated at these temperatures.
In vitro tests showed that both clones adsorbed to the phagocytes of peritoneal exudates from uninfected ferrets and nasal inflammatory exudates of ferrets infected with both clones. About 90% of the virus was adsorbed after 30 min at 0° or 370° and only 2-14% of this was recovered after treatment with receptor-destroying enzyme followed by freeze-thawing the cells. In contrast, high recoveries (36-112% of that adsorbed) were obtained from red blood cells that were treated similarly. Significant differences were not detected between the clones in either adsorption by or recovery from phagocytes of the different types of exudates.
Thus pyrexia and the nasal inflammatory cells probably play a major role in the reduction of nasal tract infection but, while pyrexia may have had some influence, no evidence was obtained to indicate that the cells contributed to the earlier reduction of Clone 64d.
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