CD-1 mice infected with a sublethal dose of influenza A virus were anesthetized for 2 h with halothane. These mice were compared to a control group which was similarly infected using ketamine sedation. Mice anesthetized with halothane showed less physical signs of illness and demonstrated less lung histopathology than the control group of mice. Virus titers were reduced in the group of animals exposed to halothane 12 h after infection, but were the same as the infected controls at all other times measured (1–12 days after infection). Morphometric analysis of lung tissue demonstrated a delayed appearance of both neutrophils and monocytes in the halothane-exposed mice. These results suggest that the halogenated volatile anesthetic halothane decreases the pulmonary pathogenesis of influenza A virus by altering the recruitment of immunological effector cells during the course of the infection.

Influenza C/Ann Arbor/1/50 was used to establish a persistent infection in Madin-Darby canine kidney cells. The persistent state has been stable for more than 4 years (over 66 passages), with infected cells differing from controls in morphology and growth characteristics. In addition, virus recovered from the media of persistent cultures (passage 58) differed from parental wild-type virus C/Ann Arbor/1/50 in (i) antigenicity by the hemagglutination-inhibition test; (ii) its ability to produce plaques in different host cells; (iii) hemagglutination of chicken erythrocytes at different temperatures; (iv) receptor-destroying enzyme activity, and (v) by sensitivity to hemagglutination inhibitors present in rat serum.