Natural infection with Marek's disease virus occurs through the respiratory mucosa after chickens inhale dander shed f r o m i n fected c h i c k e n s . The early events in the lung following exposure to the feather and squamous epithelial cell debris containing the viral particles remain unclear. In order to elucidate the virological and immunological consequences of MDV infection for the respiratory tract, chickens were infected by intratracheal administration of infective dander. Differences between susceptible and resistant chickens were immediately apparent, with delayed viral replication and earlier onset of interferon (IFN)-g production in the latter. CD4 þ and CD8 þ T cells surrounded infected cells in the lung. Although viral replication was evident in macrophages, pulmonary B cells were the main target cell type in susceptible chickens following i n t r a t r a c h e a l infection with MDV. In accordance, depletion of B cells curtailed viremia and substantially affected pathogenesis in susceptible chickens. Together the data described here demonstrate the role of pulmonary B cells as the primary and predominant target cells and their importance for MDV pathogenesis.

The history of human infections with lymphocytic choriomeningitis virus is briefly reviewed, with special reference to those of recent years associated with pet Syrian hamsters. Many human infections have been too trivial to have come to the attention of a physician but others have required long periods of convalescence. There is also evidence that foetal damage has arisen from infection during pregnancy. The virus is perpetuated by vertical transmission in those colonies of wild house mice which are tolerantly infected. These mice excrete the virus throughout life at a high titre in urine and saliva. Experimental evidence is presented which demonstrates the transfer of infection from such mice to Syrian hamsters when natural conditions are simulated. Hamsters infected before weaning may appear healthy while excreting the virus at a high titre for several months, during which they are a serious health hazard to their owners. This secondary reservoir of the virus brings the source of infection one step nearer to the veterinarian in practice, and to his clients, and he will be in a key position to inform or assist his medical colleagues if this hazard is suspected.

A new locus of wild house mice tolerantly infected with the virus of lymphocytic choriomeningitis (LCM) has been identified in the United Kingdom. Evidence is presented which indicates that these mice were the source of infection in a laboratory mouse breeding colony, the mode of transmission probably being bites on tails and limbs exposed through wire-grid flooring. The results of an experiment which simulated indirect exposure of SPF mice to tolerantly infected wild mice supported earlier observations that without injury to the epidermis the risk of spread of infection from the infective urine, saliva or faeces is low.

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