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      In utero infection with porcine reproductive and respiratory syndrome virus modulates leukocyte subpopulations in peripheral blood and bronchoalveolar fluid of surviving piglets


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          It is well known that piglets congenitally infected with porcine reproductive and respiratory syndrome virus (PRRSV) can be viremic at birth, and that preweaning mortality due to secondary infections often increases during acute outbreaks of PRRS. Therefore, an immunosuppressive effect of in utero infection has been suggested. The aim of the present study was to characterise the changes of leukocyte populations in piglets surviving in utero infection with PRRSV. A total of 27 liveborn uninfected control piglets and 22 piglets infected transplacentally with a Danish strain of PRRSV were included. At 2 and 4 weeks of age, 21 of 22 (96%) and 7 of 14 (50%) examined infected piglets were still viremic, whereas PRRSV could not be detected in the six infected piglets examined at 6 weeks of age. Flow cytometry analysis was used to determine the phenotypic composition of leukocytes in peripheral blood and bronchoalveolar lavage fluid (BALF) of 2-, 4- and 6-week-old infected piglets and age-matched uninfected controls. The key observation in the present study is that high levels of CD8 + cells constitute a dominant feature in peripheral blood and BALF of piglets surviving in utero infection with PRRSV. In BALF, the average high level of CD8 + cells in 2-week-old infected piglets (33.4±12.6%) was followed by a decline to 7.3±3.0 and 11.1±3.0% at 4 and 6 weeks of age. BALF of control piglets contained 1.6±0.9, 2.3±1.8 and 1.9±0.5% CD8 + cells, only. In peripheral blood, however, the average number of CD8 + cells remained at high levels in the infected piglets throughout the post-natal experimental period (2.8±1.9, 2.9±1.8 and 3.2±1.7×10 6 CD8 + cells/ml at 2, 4 and 6 weeks, respectively). In the controls, the average levels of CD8 + cells were 0.9±0.2, 1.9±1.7 and 1.6±0.5×10 6/ml, respectively. Furthermore, the numbers of CD2 +, CD4 +CD8 + and SLA-classII + cells, respectively, in peripheral blood, together with the levels of CD2 + and CD3 + cells in BALF were increased in the infected piglets infected in utero compared to the uninfected controls.

          The kinetic analyses carried out in the present study reflect that in utero infection with PRRSV modulates immune cell populations in peripheral blood and BALF of surviving piglets. The observed changes are characterised by high levels of CD8 + cells supporting an important role of these cells in PRRSV infection. The present results, however, do not support the existence of post-natal immunosuppression following in utero infection with PRRSV.

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          Comparison of the pathogenicity of two US porcine reproductive and respiratory syndrome virus isolates with that of the Lelystad virus.

          The Lelystad virus or one of two US isolates (VR2385, VR2431) of porcine reproductive and respiratory syndrome virus were given intranasally to 25 4-week-old cesarian-derived colostrum-deprived pigs. Pigs from these groups were necropsied at 1, 2, 3, 5, 7, 10, 15, 21, or 28 days postinoculation. The Lelystad virus and VR2431 induced mild transient pyrexia, dyspnea, and tachypnea. VR2385 induced labored and rapid abdominal respiration, pyrexia, lethargy, anorexia, and patchy dermal cyanosis. All three isolates induced multifocal tan-mottled consolidation involving 6.8% (n = 9; SEM = 3.4) of the lung for Lelystad, 9.7% (n = 9, SEM = 2.7) of the lung for VR2431, and 54.2% (n = 9, SEM = 4.4) of the lung for VR2385 at 10 days postinoculation. Characteristic microscopic lung lesions consisted of type 2 pneumocyte hypertrophy and hyperplasia, necrotic debris and increased mixed inflammatory cells in alveolar spaces, and alveolar septal infiltration with mononuclear cells. Lymphadenopathy with follicular hypertrophy, hyperplasia, and necrosis was consistently seen. Similar follicular lesions were also seen in Peyer's patches and tonsils. Lymphohistiocytic myocarditis and encephalitis were reproduced with all three isolates. Clinical respiratory disease and gross and microscopic lung lesion scores were considerably and significantly more severe in the VR2385-inoculated pigs. All three viruses were readily isolated from sera, lungs, and tonsils throughout the 28 days of the study. The lymphoid and respiratory systems have the most remarkable lesions and appear to be the major site of replication of these viruses. This work demonstrated a marked difference in pathogenicity of porcine reproductive and respiratory syndrome isolates.
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            Differentiation of U.S. and European isolates of porcine reproductive and respiratory syndrome virus by monoclonal antibodies.

            Monoclonal antibodies (MAbs) to two U.S. isolates of porcine reproductive and respiratory syndrome (PRRS) virus were prepared. Two MAbs specifically recognized a conserved epitope on the putative 15-kDa nucleocapsid protein of U.S. and European isolates of PRRS virus. Four other MAbs recognized epitopes on the 15-kDa protein of U.S. but not European isolates of PRRS virus. Collectively, this indicates that PRRS viruses contain both conserved and divergent epitopes on the 15-kDa viral protein.
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              Porcine reproductive and respiratory syndrome: clinical disease, pathology and immunosuppression.

              Porcine reproductive and respiratory syndrome (PRRS) was first known as blue-eared pig disease in the United Kingdom and the causative agent as 'Lelystad virus'. The disease is characterised by very variable clinical signs, including reproductive failure and respiratory disease. The respiratory syndrome is often associated with severe infection with secondary bacterial agents including Pasteurella multocida, Haemophilus parasuis and Streptococcus suis. However, some seropositive herds show no clinical signs of disease. The secondary infections may be facilitated by the destruction of circulating lymphocytes, by the destruction of the mucociliary clearance system and, most importantly, by a large reduction in the numbers of alveolar macrophages. The clinical syndrome observed in a herd may therefore depend in part upon the other diseases present.

                Author and article information

                Vet Immunol Immunopathol
                Vet. Immunol. Immunopathol
                Veterinary Immunology and Immunopathology
                Elsevier Science B.V.
                28 May 2003
                20 June 2003
                28 May 2003
                : 93
                : 3
                : 135-151
                [a ]Department of Virology, Danish Veterinary Institute, Lindholm, DK-4771 Kalvehave, Denmark
                [b ]Laboratory for Virology and Immunology, Department of Veterinary Microbiology, The Royal Veterinary and Agricultural University, Stigbøjlen 7, DK-1870 Frederiksberg C, Denmark
                [c ]Department of Immunology and Biochemistry, Danish Veterinary Institute, Bülowsvej 27, DK-1790 Copenhagen V, Denmark
                Author notes
                [* ]Corresponding author. Tel.: +45-558-69536; fax: +45-558-69700. jn@ 123456vetinst.dk
                Copyright © 2003 Elsevier Science B.V. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                : 15 May 2002
                : 28 January 2003
                : 13 February 2003

                Veterinary medicine
                pigs,prrsv,in utero,flow cytometry,leukocyte subpopulations,sla, swine leukocyte antigen,fsc, forward light scattering,ssc, side light scattering,balf, bronchoalveolar lavage fluid,ppam, porcine pulmonary alveolar macrophages,wbc, white blood cells,cd, cluster of differentiation


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