The present review relies upon articles published previously (1–10). Basing upon this it was the authors’ intention to consider above all additional newer literature.

Infectious Bovine Rhinotracheitis / Vulvovaginitis (BHV1)

The temporal relation between a lung infection with bovine herpesvirus-1, suppression of some immune functions, and susceptibility to secondary bacterial infection resulting in fibrinous pneumonia prompted a study to determine the mechanism(s) involved in the apparent immunosuppression. In six independent experiments employing from five to 40 calves, we studied the immunologic parameters of migration of and superoxide anion production by polymorphonuclear neutrophils, lectin-induced lymphocyte proliferation, interleukin-2 production, natural cytotoxicity, interferon and antibody formation, as well as complement activation and hematologic parameters. Chemotaxis of polymorphonuclear neutrophils, natural cytotoxicity, and mitogen response of peripheral blood leukocytes were depressed, whereas superoxide anion generation by polymorphonuclear neutrophils was transiently increased and interleukin-2 production was only marginally affected. The assumption that virus-induced interferon might be a common cause for the various changes could not be substantiated. However, the results did suggest that mechanisms other than lack of T helper cell activity, accessory cell activity of macrophages, or development of suppressor T cells were the cause of suppressed mitogen responses. None of the immunologic parameters appeared to have consistent prognostic value with respect to outcome of the infection.

Viral-bacterial pneumonia in calves: effect of bovine herpesvirus-1 on immunologic functions.

Epitope specificity of the protective immune response induced by individual bovine herpesvirus-1 glycoproteins.

The interaction between activated bovine T lymphocytes (BTLs) and bovine herpesvirus type 1 (BHV-1) was investigated. BHV-1 infection of BTLs reduced the amplitude of recombinant bovine interleukin 2-induced proliferative responses. This decreased proliferation was caused by a virus-induced lymphocytolysis which was dependent on viable virus and was not inhibited by recombinant bovine interferon-α11. Furthermore, lymphocytolysis was not associated with virus replication or with the synthesis of detectable levels of viral proteins. Electron microscopic examination of virus-infected cells revealed that lymphocytolysis was characterized by early nuclear disintegration resembling apoptosis. These observations suggest that activated T cells, localized at the site of BHV-1 infection, may be susceptible to virus-induced cytolysis.

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes.

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.

/pdf/viral-bacterial-synergistic-interaction-in-respiratory-26yngh9d42.pdf

Viral-bacterial synergistic interaction in respiratory disease.

The effect of bovine herpesvirus type 1 on the specific and nonspecific immune response of calves was examined. Animals with or without prior aerosol exposure to Pasteurella haemolytica serotype A1 were aerosol challenged with 10(8) PFU of virus. Blood and serum samples were taken before and after virus challenge for determining cell-mediated, humoral, and neutrophil responses. A significant depression of the blastogenic responses to phytohemagglutinin, P. haemolytica, and Pasteurella multocida and of neutrophil chemotactic response was observed 4 to 7 days after challenge. However, the antibacterial activity of neutrophils was not significantly affected by virus exposure. Anti-bovine herpesvirus type 1 antibody responses were detected 11 days postchallenge. A significant elevation of the anti-P. haemolytica antibody response (day 0 versus day +11) was detected in animals previously exposed to P. haemolytica.

Nonspecific suppressive effect of bovine herpesvirus type 1 on bovine leukocyte functions.

Nonspecific Suppressive Effect ofBovineHerpesvirus Type1 on Bovine Leukocyte Functionst

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Nonspecific suppressive effect of bovine herpesvirus type 1 on bovine leukocyte functions.

Nonspecific Suppressive Effect ofBovineHerpesvirus Type1 on Bovine Leukocyte Functionst