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On farms, where the porcine respiratory coronavirus (PRCV) is enzootic, pigs usually become infected between 5 and 10 weeks of age while losing their maternal antibodies. It was examined whether PRCV replicates in the small intestine in such pigs. This point is important since intestinal replication with PRCV might induce immunity against TGEV not only by stimulating mucosal intestinal immunity, but also by the induction of a lactogenic IgA response at later age via the gut-mammary link. Five week old pigs with and without maternal antibodies were inoculated by aerosol or directly into the intestinal lumen. In aerosol inoculated pigs, virus replication was observed to high titres in the respiratory tract. Replication occurred in epithelial cells of nasal mucosa, trachea, bronchi bronchioli and alveoli and in alveolar macrophages. Small amounts of virus produced in the respiratory tract were ingested, but no intestinal replication of PRCV was demonstrated. Differences were not observed in virus titre and sites of replication in seronegative pigs compared to those in pigs with maternal antibodies. Upon inoculation of 10(5) or 10(7) TCID50 directly into the lumen of the cranial jejunum, no intestinal replication could be demonstrated.

Three strains of human coronavirus (HCV) OC43 were compared for their ability to cause enteric infections and to induce interferon alpha (IFN alpha) using the Caco-2 human colon carcinoma cell line which exhibits spontaneous epithelial differentiation in vitro. MRC-5 cell culture grown stocks were prepared from: 1. CV Paris, a strain of OC43 recovered from an outbreak of necrotizing enterocolitis in newborns. 2. CV Mb, a neurotropic strain of OC43 which exhibits strict neuronal specificity in murine neuronal cell cultures. 3. CV Rd, a strain of OC43 which grows to a high titer in human rhabdomyosarcoma (RD) cells. Immunofluorescent staining for nucleocapsid antigen and plaque assay in MRC-5 cells was used to detect viral replication. BG-9 (human foreskin) cells challenged with vesicular stomatitis virus were used to detect IFN alpha production by human peripheral blood monocytes (PBMC) stimulated by virus infected Caco-2 cells. Caco-2 cells infected with virus at a multiplicity of infection of 0.5 yielded 10(4.6) and 10(4.4) plaque forming units/ml (pfu/ml) with CV Rd and CV Paris respectively, while CV Mb yielded only 10(3) pfu/ml. Caco-2 cells infected with CV Rd induced 64 IU/ml of IFN alpha in PBMC while these cells infected with CV Paris induced less than 2 IU/ml IFN alpha. In cells infected with CV Mb 4 IU/ml IFN alpha was detected. The results suggest that a lack of IFN alpha induction by CV Paris may be an indicator of its enteropathogenic potential.(ABSTRACT TRUNCATED AT 250 WORDS)