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Adult bovines, young calves and young rats were infected with bovine herpes mammillitis (BHM) virus providing a group of BHM-recovered animals in which to investigate a possible latent carrier state. The progression of the acute infection and serological response was essentially similar to that previously reported. The effect of natural (calving, littering) and artificial (corticosteroid treatment) stress on these animals following recovery from infection was investigated, but reactivation of BHM was never detected. Long term observation of cocultures of BHM virus infected-and-recovered bovine teat dermis with bovine embryo cells failed to reveal any evidence for the induction of BHM virus replication even in those cocultures treated with mitomycin C or bromodeoxyuridine. Similarly, cocultures utilizing lumbar dorsal root ganglia from the same animals were also negative with respect to the induction of virus replication. Experiments using cytosine arabinoside indicated that an artificial in vitro latent carrier state of BHM virus could be maintained for 6 days with subsequent sporadic virus reactivation, but an attempt to maintain such a state for 12 days was unsuccessful, with no subsequent virus reactivation.

Cells washed from the lungs of freshly killed calves (lung wash cells; LWC) were cytotoxic for calf kidney (CK) target cells infected with parainfluenzavirus type 3 (Pi-3) when assayed by chromium release. LWC collected from 25 calves, including two gnotobiotic animals that had not previously been infected with Pi-3, were all cytotoxic, giving a specific chromium release between 11 and 50%. Cytotoxicity was detected at ratios of LWC to target cell as low as 5:1. The cytotoxic reaction required viable LWC, was inhibited by Pi-3 antiserum, and was not the result of virus-induced damage to the target cells. The cytotoxic cells in the LWC population were identified as alveolar macrophages from observations on glass adherence, phagocytic activity, killing by silica and fine-structural appearance. When LWC were added to CK cells or organ cultures of bovine trachea infected with Pi-3, the yield of virus was reduced for the first 2 to 3 days. However, subsequently, Pi-3 virus replicated in the LWC. Infection of LWC with Pi-3 virus reduced their cytotoxic activity. The significance of these interactions between alveolar macrophages and Pi-3 virus is discussed.

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