SUMMARYAntigenic relatedness between the virion-associated proteins of caprine arthritisencephalitis, visna and progressive pneumonia viruses was examined. Antigenic crossreactivity was assessed by immunoprecipitation of disrupted, radiolabeUed virus with goat, sheep and rabbit antisera, followed by resolution of the immunoprecipitation products by SDS-polyacrylamide gel electrophoresis. The results indicate that antigenic cross-reactivity between the caprine and ovine virus isolates involves all of the major virion-associated proteins and glycoproteins. The common antigenic determinants exhibited by virion structural proteins are immunogenic in goats, sheep and rabbits.

The mesenteric microvasculature was studied in rats and rabbits infected with Trypanosoma congolense. By examining vessels in the living animals, trypanosomes were observed to adhere to vessel walls by their anterior ends. It was evident from stained preparations of the vessels that the microcirculation contained 4-1400 times as many trypanosomes as were free in the cardiac blood. Parasites were more numerous in very small vessels than in larger vessels, and they were clustered in groups within the small vessels. The localization of T. congolense in the microvasculature is demonstrated and it is shown that this localization is established by attachment of the organism to the vessel wall.

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Trypanosoma congolense binds to erythrocytes and the walls of the microvasculature. Experiments were conducted to determine if the attachment of T. congolense, alone or in combination with antitrypanosome antibody, was damaging to host cells. Bovine erythrocytes were labelled with 51Cr and incubated with T. congolense to promote adhesion. Plasma from the same donor as the red blood cells was added to the erythrocyte-trypanosome aggregates and the release of 51Cr measured. There was a two- to threefold increase in 51Cr release when trypanosomes were lysed by antibody-complement interaction following adhesion to the erythrocyte. The erythrocytes were not damaged by trypanosome binding in the absence of antibody or complement. A similar mechanism may operate in vivo because experiments demonstrated an increased vascular permeability of mesenteric vessels, a site of T. congolense attachment to the microcirculation. These results suggest that the adhesion of T. congolense to host cells, followed by an immune response to the parasite, may damage the infected host by "innocent bystander" mechanisms.

Trypanosoma congolense Broden, an intravascular parasite, binds to vessel walls and erythrocytes of infected hosts. In an attempt to characterize T. congolense adhesion to host cells, an in vitro assay was devised. It was shown in the in vitro experiments that T. congolense binds to bovine, sheep, and goat erythrocytes, but not always to erythrocytes of rats, mice, rabbits, horses or humans. Only the anterior part of live trypanosomes adheres to erythrocytes, and the attachment site on the trypanosomes is destroyed by trypsin and chymotrypsin-trypanosomes did not adhere to bovine erythrocytes that had been incubated with neuraminidase, sodium periodate and poly-L-lysine. The foregoing experiments suggest that the surface of T. congolense contains a protein-associated site which binds to sialic acid of some host cells. This surface site is most likely responsible for attachment to blood vessels in vivo.

Macrophages are a major component of the arthritic lesions induced by the lentivirus caprine arthritis-encephalitis virus (CAEV). Using autoradiography and the appearance of mitotic figures to detect dividing macrophages, we found that 2.1% +/- 0.2% of synovial fluid macrophages from uninfected goats are dividing and that after infection with CAEV the percentage increases three- to sixfold. The enhanced macrophage division was not associated with increased dividing of blood monoblasts. The amount of macrophage division correlated with two measures of arthritis: joint swelling and the number of synovial fluid macrophages. Induction of an immune response in the joints of CAEV-infected goats increased the number of dividing macrophages. The synovial fluid of infected animals was mitogenic for macrophages from infected animals in amounts that correlated with the amount of macrophage division occurring in the joints. Activated lymphocytes produced nondialyzable lymphokines mitogenic for macrophages from CAEV-infected goats but not from uninfected goats. These results suggest that in situ macrophage division contributes to the lesions induced by CAEV and that infection leads to greater responsiveness of macrophages to mitogenic factors produced by lymphocytes.

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