Immunopathology of chickens infected in vivo and at hatching with the avian osteopetrosis virus MAV.2–0

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Abstract
The immunological capacity of chickens infected with MAV.2–0, an avian osteopetrosis virus, was studied both morphologically and functionally. Infection of 11 to 12‐day‐old embryos with a high (0.58 × 106‐1.2 × 106 plaque‐forming units; PFU) and an intermediate (5.8 × 104 PFU) dose of virus resulted in severe stunting, as manifested by lower body and lymphoid organs (bursa, thymus and spleen) weights. The bursa and spleen of osteopetrotic chickens were poorly developed, the thymus partially necrotized; all lymphoid organs had fewer lymphocytes than controls, and there were far fewer germinal centers in the spleen of infected birds, as compared to controls. The humoral and cellular immunity of these osteopetrotic chickens was significantly suppressed, as assessed by (a) the plaque‐forming cell response against sheep red blood cells (SRBC) in the spleen; (b) circulating antibody responses against SRBC, Brucella abortus and human γ‐globulins (HGG); (c) the delayed hypersen‐sitivity reaction against HGG; and (d) mitogenic responsiveness of peripheral blood and spleen lymphocytes to concanavalin A, phytohemagglutinin M and pokeweed mitogen. A few birds, infected as 11‐day embryos with the lowest concentration of virus (2.9 × 104 PFU) had no palpable bone lesions, the lymphoid organs had normal histology, and immune responses were quite similar to those in uninfected control birds. Osteopetrotic chickens, infected within 48 h after hatching (5.8 × 105 PFU), had normal IgM‐class antibody responses against all antigens studied (SRBC, Brucella, HGG), whereas IgG and/or IgA responses tended to be lower than those observed in the normal controls. These findings, together with the regularly organized small lymphoid follicles in the bursa, indicate a late affection of B cell development, whereas in the birds infected at 11–12 days of incubation, an almost total arrest of B cell development was observed. T cell functions of birds infected at hatching were suppressed to the same extent as those of in ovo infected birds indicating susceptibility of the T cell lineage to MAV.2–0 also at later stages of development.