Abstract
Although viral illnesses are predisposing causes for pulmonary bacterial infections, the interrelationships of viral virulence and host immunity to alterations in susceptibility to bacterial infection are incompletely understood. We used two mutant strains of encephalomyocarditis virus (minimally virulent Mengo-37A and a highly virulent Columbia SK [Col-SK]) to investigate these interrelationships. Mice that had been immunized to Mengo-37A, and nonimmunized controls, were challenged with aerosols containing 10(4) plaque-forming units of Mengo-37A or Col-SK per liter. The effect of each viral infection on pulmonary antibacterial activity was assessed 3 days later by measuring the capacity of the lungs to kill inhaled radiophosphorus ((32)P)-labeled Staphylococcus aureus. The degree of antibacterial dysfunction found was proportional to the virulence of the infecting virus. If the host was immune to the infecting virus, bactericidal function was not impaired by viral challenge. Neither mutant caused significant pulmonary damage; therefore: (i) viral-induced impairment in bactericidal activity reflects, quantitatively, the virulence of the virus and (ii) viral immunity protects pulmonary bacterial defenses by preventing damage to the phagocyte from the virus or its attendant metabolic abnormalities.