Phenotype and Function of CD209+ Bovine Blood Dendritic Cells, Monocyte-Derived-Dendritic Cells and Monocyte-Derived Macrophages.

Phylogenic comparisons of the mononuclear phagocyte system (MPS) of humans and mice demonstrate phenotypic divergence of dendritic cell (DC) subsets that play similar roles in innate and adaptive immunity. Although differing in phenotype, DC can be classified into four groups according to ontogeny and function: conventional DC (cDC1 and cDC2), plasmacytoid DC (pDC), and monocyte derived DC (MoDC). DC of Artiodactyla (pigs and ruminants) can also be sub-classified using this system, allowing direct functional and phenotypic comparison of MoDC and other DC subsets trafficking in blood (bDC). Because of the high volume of blood collections required to study DC, cattle offer the best opportunity to further our understanding of bDC and MoDC function in an outbred large animal species. As reported here, phenotyping DC using a monoclonal antibody (mAb) to CD209 revealed CD209 is expressed on the major myeloid population of DC present in blood and MoDC, providing a phenotypic link between these two subsets. Additionally, the present study demonstrates that CD209 is also expressed on monocyte derived macrophages (MoΦ). Functional analysis revealed each of these populations can take up and process antigens (Ags), present them to CD4 and CD8 T cells, and elicit a T-cell recall response. Thus, bDC, MoDC, and MoΦ pulsed with pathogens or candidate vaccine antigens can be used to study factors that modulate DC-driven T-cell priming and differentiation ex vivo.

Immunoblotting analysis of the reaction of wildebeest, sheep and cattle sera with the structural antigens of alcelaphine herpesvirus-1 (malignant catarrhal fever virus).

Malignant catarrhal fever (MCF) is a disease of cattle and some other ruminants caused by alcelaphine herpesvirus-1 (AHV-1), a virus of wildebeest. The disease also occurs in the absence of wildebeest and is then thought to be caused by a viral agent harboured by the sheep. The structural proteins of AHV-1 have been used as antigens for the immunoblotting analysis of sera from wildebeest, sheep and cattle infected by either AHV-1 or the "sheep-associated" form of the disease. Wildebeest sera showed a uniform response reacting strongly with six polypeptides. Sheep sera also gave positive results but individual sera reacted with varying subsets of the antigens recognized by wildebeest. These results support the earlier suggestion that sheep harbour a herpesvirus related to AHV-1. A bovine serum from a case of MCF caused by AHV-1 also reacted only with a subset of the six wildebeest-reactive polypeptides. Sera from cattle affected with the "sheep-associated" form of the disease gave reactions in only two of the eight cases tested; both positive sera reacted to a few polypeptides only.

Phylogenetic distribution of a 24,000 dalton human leukemia-associated antigen on platelets and kidney cells.

The distribution of a 24,000-dalton human leukemia-associated antigen, p24, was examined using the BA-2 and DU-ALL-1 monoclonal antibodies. BA-2 and DU-ALL-1 bound to human, gorilla, orangutan, macaque, and rabbit platelets but did not bind to mouse, rat, guinea pig, dog, horse, sheep, or goat platelets. Orangutan platelets demonstrated a decreased level of binding with BA-2 and DU-ALL-1. In addition, BA-2, but not DU-ALL-1, bound to chimpanzee platelets suggesting that the chimpanzee has lost the epitope of p24 detected by DU-ALL-1. Immunoperoxidase analysis of kidney tissue with BA-2 and DU-ALL-1 revealed staining of distal tubules and glomeruli, which occurred in a similar phylogenetic distribution to that of p24 on platelets. A monoclonal antibody to the high molecular weight common ALL antigen, J-5, reacted with glomeruli and proximal tubules from human, chimpanzee, orangutan, mangaby , rhesus, and rabbit kidneys but failed to react with rat or mouse kidney.

Antibodies in carrier wildebeest to the lymphoproliferative herpesvirus of malignant catarrhal fever.

Six types of antibody to malignant catarrhal fever virus (MCFV) were measured in 132 sera collected from Wildebeest in Kenya Masailand. The titre of all types of antibody declined slowly with increasing age of the wildebeest. A significantly greater proportion of wildebeest calves had higher titres of antibodies to MCFV early antigens, IgM antibodies to MCFV late antigens and complement-fixing antibodies, than did older animals. One seronegative calf, reared in isolation without colostrum, became seropositive 4 1/2 weeks after birth but did not show any clinical signs indicative of MCFV infection. Similarities between MCFV infection of wildebeest calves and other inapparent infections with lymphoproliferative herpesviruses are discussed.

Malignant catarrhal fever virus specific secretory IgA in nasal secretions of wildebeest calves.

Wildebeest IgA was isolated from nasal secretions and precolostrum. It was identified by cross-reaction with anti-human and anti-bovine IgA sera. Nasal secretions collected from wildebeest calves over 3 months old had malignant catarrhal fever virus neutralizing antibody activity. They also contained specific IgA to the virus as detected by indirect immunofluorescence. It is suggested that production of malignant catarrhal fever virus specific IgA in the nasal cavity, contributes to the elimination and cessation of the virus shed in the nasal secretions of wildebeest calves over 3 months. old.

Enzyme-linked protein A: an enzyme-linked immunosorbent assay reagent for detecting antibodies in tuberculous exotic animals.

An enzyme-linked immunosorbent assay (ELISA) was developed, using protein A labeled with horseradish peroxidase for detecting antibodies in tuberculous exotic mammals (llamas, rhinoceroses, elephants). The modified ELISA provides a rapid procedure for screening several animal species simultaneously for tuberculosis without the production of specific anti-species conjugates. Heat-killed cells of Mycobacterium bovis and M avium and purifed protein-derivative tuberculin of M bovis were used as antigens for ELISA.

A seroepidemiologic survey of three pronghorn (Antilocapra americana) populations in southeastern Idaho, 1975-1977.

Sera from 104 adult and 42 fawn pronghorn antelope (Antilocapra americana) from southeastern Idaho were tested against selected livestock pathogens. The numbers positive/numbers tested (% positive) were as follows: bovine virus diarrhea - adults 2/102 (2), fawns 0/41 (0);; infectious bovine rhinotracheitis - adults 27/101 (27), fawns 9/42 (22); parainfluenza 3 - adults 79/104 (76), fawns 22/42 (52); bovine adenovirus 7 - adults 42/103 (41), fawns 20/48 (48); bovine adenovirus 3 - adults 11/32 (34), fawns 4/14 (23); Anaplasma marginale - adults 1/104 (1), fawns 1/42 (2). There were no reactors to brucellosis, bluetongue, or epizootic hemorrhagic disease; The prevalence of reactors varied considerably for different locations and for different years.

Neutralising antibody to herpesviruses dervied from wildebeest and hartebeest in wild animals in East Africa.

The sera of 728 game animals, collected in East Africa, were tested for neutralising antibody to a strain (WC11) of wildebeest herpesvirus, which is an important cause of malignant catarrhal fever of cattle. In addition, 290 of these sera were tested for neutralising activity against a closely related herpesvirus (K/30) from hartebeest (Alcelaphus sp.). Antibody was frequently present in three species of the subfamily Alcelaphinae (wildebest, hartebeest and topi) and one of the subfamily Hippotraginae (oryx). No activity was found in the sera of nine other species of four additional subfamilies. The proportion of hartebeest sera positive for WC11 virus (60 per cent) was not significantly different from that neutralising the K/30 isolate (77 per cent) and antibody titres against the two agents did not differ significantly. Of 62 topi sera 40 per cent neutralised WC11 virus, while all of three oryx sera were positive. It is suggested that the antibody detected in hartebeest, topi and oryx was induced by infection with viruses related to, but not identical with, the WC11 and K/30 strains. Some characteristics of the latter indicated that it was not the usual herpesvirus of hartebeest and may have been derived from wildebeest. It is proposed that the group of viruses involved should be provisionally designated as 'alcelaphine herpesviruses' in order to separate them from the rest of the 'bovid' herpesviruses, a name proposed by the Herpesvirus Sbucommittee of the International Committee on the Nomenclature of Viruses.