Viral-bacterial synergistic interaction in respiratory disease.

In the present review we have identified how viruses can alter the host's susceptibility to bacterial infections by altering both environmental conditions in the lung which favor bacterial replication as well as by suppressing the host's defense mechanisms which prevent clearance of the bacteria. In many instances, these interactions are extremely complex but similar for many viruses. If the virus can overcome the initial host defense mechanisms, which include local antibody and mucus, the virus initiates tissue damage as a result of direct replication within the epithelial cells lining the mucosal surfaces of the respiratory tract. As a result of virus infection, the host cells respond by producing a variety of mediators including various types of interferons, which can alter both virus replication and host response. Replication also produces by-products of virus infection capable of initiating an inflammatory process, which in turn, through release of other mediators, can further modify lung defense mechanisms and encourage bacterial adherence and growth. The bacterium, in turn, releases chemotactic factors which encourage infiltration of specific effector cells into the lung. These effector cells can cause tissue damage and immunopathology, which encourage rapid bacterial growth and may result in death of the animal. In order to be able to control this complicated scenario, it is important either to prevent the initial infection with viruses or to reduce the degree of immunosuppression, so that bacterial clearance can occur rapidly before microcolony formation and extensive lung damage occur. Once a large amount of bacterial replication and lung damage is present, the use of antibiotics is generally of limited value. A schematic illustration of the complexity of the various interactions and counteractions occurring during virus--bacterial synergistic interactions is presented in Fig. 1.