In situ detection of ovine progressive pneumonia virus (OPPV) and the phenotypic identification of the cells that harbor OPPV have not been described for the OPPV-affected tissues, which include lung, mammary gland, synovial membranes of the carpal joint, and choroid plexus of the brain. In this study, the authors first developed a single enzyme-based automated immunohistochemical (IHC) analysis for detection of OPPV capsid antigen (CA) on OPPV-affected tissues, using 2 anti-CAEV CA monoclonal antibodies, 5A1 and 10A1, and 2 enzyme-based IHC systems. Out of 10 naturally and persistently OPPVinfected ewes, OPPV CA was detected in intercellular regions of the carpal synovial membrane of 1 ewe, in cells resembling alveolar macrophages and pulmonary interstitial macrophages in lung tissue of 3 ewes, and in mammary alveolar cells of 1 ewe. Furthermore, dual enzyme-based automated IHC analyses revealed that OPPV CA was predominantly detected in CD172a-or CD163-positive alveolar macrophages of the lungs and mammary gland. That anti-inflammatory (CD163) and downregulatory (CD172a) types of alveolar macrophage harbor OPPV CA leads to the possibility that during persistent infection with OPPV, the host alveolar macrophage might serve to limit inflammation while OPPV persists undetected by the host adaptive immune response in the lung and mammary gland.Keywords ovine progressive pneumonia virus, maedi-visna virus, ovine lentivirus, capsid, dual immunohistochemistry, CD163, CD172aThe small ruminant lentiviruses (SRLVs), including ovine progressive pneumonia virus (OPPV), maedi-visna virus (MVV), and caprine arthritis-encephalitis virus (CAEV), are phylogenetically similar and are part of the Retroviridae family, which includes human immunodeficiency virus (HIV).
54Clinical signs of SRLV include dyspnea, firmness of the udder and/or reduced milk production (mastitis), swollen joints and lameness (arthritis), cachexia, and ataxia. Clinical signs can vary in animals; therefore, the reference standard for evaluating the extent of disease caused by SRLVs is postmortem histological assessment of lung, mammary gland, carpal synovial membrane, and choroid plexus. 7,11,13 Definitive diagnosis of SRLV infection cannot be made on the sole basis of histopathology; as such, serological (enzyme-linked immunosorbent assay [ELISA]) and/or molecular (polymerase chain reaction [PCR]) diagnostic tests are used to establish the presence of infection.
15The SRLVs are considered immunopathological diseases, meaning that subsequent immune responses to the virus are thought to contribute more to the pathology of the disease than to the virus alone. 12 The histological progression of SRLV-induced pathology in the tissues is thought to follow a general pattern whereby there is increased lymphoid follicle development and mononuclear and plasma cell infiltration, as followed by edema and necrosis of tissues in severe cases. In MVV-infected sheep, more MHC class II-positive cells and CD8-positive cells are observed in the bronchoalveolar lavage...