SUMMARYPigs were infected by the intranasal instillation of a large dose (ca. 107·0 ID 50) of a highly virulent strain of African swine fever virus (ASFV) and the progress of the infection was studied by the ‘routine titration approach’ (Mims, 1964) using pig bone marrow cultures.Virus growth was established within 16–24 hr. in the retropharyngeal but not in the alimentary or nasal mucosae or the tonsils. By 24–40 hr. the virus was consistently present in the retropharyngeal lymph nodes, almost invariably the medials; titres in these nodes exceeded those in the associated mucosa by 48–72 hr. Generalization, presumed to have occurred via the tracheal lymph ducts and the blood stream, was generally demonstrable after 72 hr., i.e. by the time of the onset of pyrexia or 24 hr. prior to this.On average 11% of the total infectivity in the blood was present in the plasma, with the rest assumed to be cell-associated. A mean of about 45% of the total infectivity was recovered in erythrocyte fractions in which the concentration of leucocytes had been materially reduced; fractions with increased leucocyte counts contained relatively little virus and it was concluded that the great majority of circulating virus was closely associated with the erythrocytes. Adsorption of ASFV to normal pig erythrocytes was demonstrated in vitro.The greatest concentrations of virus were recorded in the lymph nodes, especially those of the cephalic region, and in the spleen, where titres commonly attained 108·0 to 109·0 HAD 50/g. and exceeded those in the blood. They were, therefore, thought to be the source of much circulating virus, although there was some evidence that the liver, lungs and bone marrow may also have contributed, at least in some animals. There was no evidence that the mucosae of the alimentary and respiratory tracts or the kidney, myocardium and brain were a source of significant amounts of virus. The virus demonstrable in Peyer's patches did not exceed that in the intervening ileal mucosa.Although contact transmission of ASF does not normally occur during the first 12–24 hr. of fever, considerable amounts of virus were usually present in the nasal and intestinal mucosae at 72 hr. It was probable that this infectivity was due to the blood content and that excretion did not occur until the epithelium was breached.Three pigs, all of which had lesions of a portal cirrhosis, showed a delayed or restricted generalization of virus, in comparison with the other twenty-eight animals which behaved according to a regular pattern.We are grateful to Mrs M. O'Sullivan and Mrs E. Douglas for painstaking technical assistance and to Mr C. S. Rampton, A.I.M.L.T., for the preparation of the figures.

Cattle were infected with rinderpest virus by housing them for 24 hr. in stalls containing donor animals which had been reacting to the disease for 3–5 days. They were then transferred to individual clean stalls and killed on the 2nd to 10th days following first exposure. Various tissues were collected, particularly those of the upper and lower respiratory tracts, and their virus content was estimated in calf-kidney tissue cultures.Virus was recovered from 15 of 35 animals tested and in eight of these generalization had occurred, although only two had begun to show a pyrexial response. The stage of the infection could not be predicted from the time that had elapsed following exposure, since early, limited proliferation was encountered on the 3rd to the 10th days.It was considered that seven animals gave indications of the pathways by which natural infection had occurred. In each of these virus proliferation was established very early in the pharyngeal lymph node; in three the submaxillary lymph node was similarly involved and in four the palatal tonsil. It was suggested that these data probably indicated that infection always occurred via the upper respiratory tract.In three cases virus titres were highest in the bronchial or costocervical lymph nodes; this was construed as evidence for the additional involvement of the lower respiratory tract in primary infection.No infectivity could be demonstrated in the mucosae or lung parenchyma associated with the above-mentioned lymph nodes and this, together with previously published data, was accepted as strong presumptive evidence that the infecting virus passes through the mucosae without producing a local lesion or proliferating there. These results were compared briefly with those of Bedson & Duckworth (1963) for rabbit pox.

Synthetic peptides based on the VP1 proteins of two serotypes of foot-and-mouth disease virus (FMDV) and having the general formula C-C-(200-213)-P-P-S-(141-158)-P-C-G induce heterologous as well as homologous protection against challenge. Substitution of the sequence consisting of residues 200 to 213 (200-213 sequence) with a second copy of the homologous 141-158 sequence (i.e., homodimers) resulted in failure of either serotype peptide to protect heterologously. The antiviral and antipeptide titers of sera from guinea pigs immunized with the homodimeric 141-158 peptides showed serotype specificity and, with the data from the heterodimeric peptide vaccines, suggested that the C-terminal 141-158 sequence was more effectively recognized by the immune system than the N-terminal sequence. Whereas heterologous antiviral titers as measured by enzyme-linked immunosorbent assay and virus neutralization tests have not been observed with sera from cross-protected animals, epitope-mapping studies established that there was heterologous recognition of an octapeptide within the 200-213 sequence. That the 200-213 sequence was required for the induction of heterologous protection was also confirmed with a number of peptides, including hybrids based on the 200-213 sequence of one virus and the 141-158 sequence of a second virus. Thus, peptides of the general formula given above induce serotype-specific and serotype-cross-reactive protective antibodies and are unique in their induction of significant levels of heterologous protection, a property which has never been reported for whole FMDV vaccines.

The presence of either thiosulphate-neutralized or free AEI was shown to degrade inactivated foot-and-mouth disease virus Type O (Hong Kong) antigen during storage at 4 degrees C. Deterioration was evident after 20 weeks of storage and little antigen remained at 36 weeks. Optimum stability was obtained by removing the residual inactivant immediately after inactivation.

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