Effect of PRRSV Infection on MHC Expression by Macrophages and Monocytes

Porcine reproductive and respiratory syndrome virus (PRRSV) is a recent and widespread pathogen in the U.S. swine population. PRRSV infects cells of the macrophage/ monocyte/dendritic lineages which are important antigen presenting cells (APCs) of the immune system. Using flow cytometric (FACs) analysis, we demonstrated that PRRSV infection decreases the expression of the major histocompatibility complex (MHC) glycoproteins on the cell surface of infected macrophages. This decrease in MHC protein expression may reduce the ability of the macrophages to present viral antigens to the appropriate lymphocytes. The potential lack of viral antigen presentation may play a crucial role in the persistent viremia observed in PRRSV-infected pigs

An Experimental Model for Porcine Circovirus Type 2 and Mycoplasma hyopneumoniae Co-infection

Sixty-seven pigs were randomly assigned to four groups. Group 1 served as negative control pigs, group 2 pigs were inoculated with Mycoplasma hyopneumoniae (M. hyopneumoniae), group 3 pigs were dually-inoculated with M. hyopneumoniae and porcine circovirus type 2 (PCV2) and group 4 pigs were inoculated with PCV2. Dual-infected pigs had moderate dyspnea, lethargy, and reduced weight gain. The overall severity of PCV2- associated microscopic lesions in lung and lymphoid tissues were significantly (p\u3c0.05) higher in the dualinfected pigs compared to all other pigs. Four of 17 dual infected pigs had lesions consistent with postweaning multisystemic wasting syndrome (PMWS) whereas none of the singular PCV2-infected pigs developed PMWS. This study indicates that M. hyopneumoniae potentiates the severity of PCV2-associated lesions and increases the incidence of PMWS. This co-infection model closely mimics the field situation were co-infections with PCV2 are commonly observed. In the future this model will be very useful for testing intervention strategies for the control of PCV2-associated disease in growing pigs

Issues encountered in development of enzymelinked immunosorbent assay for use in detecting \u3ci\u3eInfluenza A virus\u3c/i\u3e subtype H5N1 exposure in swine

A potential mechanism by which highly pathogenic avian Influenza A virus subtype H5N1 could more readily infect human beings is through the infection of and adaptation in pigs. To detect the occurrence of such infection, monitoring of pig populations through serological screening would be highly desirable. In the current study, hemagglutination inhibition assays were able to detect antibodies against H5N1 developed in pigs, but because of antigenic variation between clades, the use of multiple virus strains were required. Whole recombinant virus and recombinant hemagglutinin antigen enzymelinked immunosorbent assays (ELISAs) were generated that could detect antibody against multiple H5N1 strains, but which also detected antibody against endemic swine influenza viruses. A recombinant hemagglutinin antigen-based ELISA was as effective as the whole virus antigen ELISAs in detecting antibody against the H5N1 virus strains used and eliminated nearly all of the cross-reactivity with non-H5N1 virus antibody. The current study also highlighted the difficulty in establishing a decision (cutoff) value that would effectively counterbalance nonspecific reactivity against sensitivity. The results provide important information and considerations for the development of serological screening assays for highly pathogenic avian H5N1 viruses

Antibody responses following vaccination versus infection in a porcine circovirus-type 2 (PCV2) disease model show distinct differences in virus neutralization and epitope recognition

Porcine circovirus associated disease (PCVAD) encompasses a group of syndromes linked to infection with porcine circovirus type 2 (PCV2). Based on the hypothesis that the immune responses to vaccination versus infection are quantitatively and qualitatively different, the objective of this study was to evaluate immunity, virus replication and disease protection in pigs vaccinated with PCV2 capsid protein (CP) and during infection. The disease model included dual infection with PCV2 and porcine reproductive and respiratory syndrome virus (PRRSV), a virus known to enhance disease progression and severity. The principal effect of PRRSV infection was to increase peak PCV2 viremia by almost 40-fold; however, PCV2 failed to show a reciprocal effect on PRRSV. In vaccinated pigs, there was no evidence of disease or PCV2 replication following dual virus challenge. Immunity following vaccination favored PCV2 neutralizing activity; whereas, PCV2 infection and disease produced high levels of non-neutralizing antibody, primarily directed against a polypeptide in the C-terminal region of CP. These results support the notion that the magnitude of the total antibody response cannot be used as a measure of protective immunity. Furthermore, protection versus disease lies in the immunodominance of specific epitopes. Epitope specificity should be taken into consideration when designing PCV2 vaccines

Clinical and pathological responses of pigs from two genetically diverse commercial lines to porcine reproductive and respiratory syndrome virus infection

The response to infection from porcine reproductive and respiratory syndrome virus (PRRSV) for 2 genetically diverse commercial pig lines was investigated. Seventy-two pigs from each line, aged 6 wk, were challenged with PRRSV VR-2385, and 66 litter-mates served as control. The clinical response to infection was monitored throughout the study and pigs were necropsied at 10 or 21 d postinfection. Previous analyses showed significant line differences in susceptibility to PRRSV infection. This study also revealed significant line differences in growth during infection. Line B, characterized by faster growth rate than line A in the absence of infection, suffered more severe clinical disease and greater reduction in BW growth after infection. Correlations between growth and disease-related traits were generally negative, albeit weak. Correlations were also weak among most clinical and pathological traits. Clinical disease traits such as respiratory scores and rectal temperatures were poor indicators of virus levels, pathological damage, or growth during PRRSV infection. Relationships between traits varied over time, indicating that different disease-related mechanisms may operate at different time scales and, therefore, that the time of assessing host responses may influence the conclusions drawn about biological significance. Three possible mechanisms underlying growth under PRRSV infection were proposed based on evidence from this and previous studies. It was concluded that a comprehensive framework describing the interaction between the biological mechanisms and the genetic influence on these would be desirable for achieving progress in the genetic control of this economically important disease

Effect of PRRSV Infection on MHC Expression by Macrophages and Monocytes

Porcine reproductive and respiratory syndrome virus (PRRSV) is a recent and widespread pathogen in the U.S. swine population. PRRSV infects cells of the macrophage/ monocyte/dendritic lineages which are important antigen presenting cells (APCs) of the immune system. Using flow cytometric (FACs) analysis, we demonstrated that PRRSV infection decreases the expression of the major histocompatibility complex (MHC) glycoproteins on the cell surface of infected macrophages. This decrease in MHC protein expression may reduce the ability of the macrophages to present viral antigens to the appropriate lymphocytes. The potential lack of viral antigen presentation may play a crucial role in the persistent viremia observed in PRRSV-infected pigs.</p

Lung inflammatory responses

Inflammation is an important manifestation of respiratory disease in domestic animals. The respiratory system is mucosal in nature and has specific defense mechanisms used to control invasion by microbes and environmental elements. Inflammation can be beneficial or detrimental to the host. This article broadly discusses the primary mediators and mechanisms of inflammation within the respiratory tract of domestic animals. The role of cells, chemokines, cytokines and mediators in both acute and chronic inflammation are addressed. The pathogenesis of the initial insult determines the type of inflammation that will be induced, whether it is acute, chronic or allergic in origin. Maintenance of the microenvironment of cytokines and chemokines is critical for pulmonary homeostasis. Uncontrolled inflammation in the respiratory tract can be life threatening to the animal. The understanding of the mechanisms of inflammation, whether due to microbes or through inappropriate immune activation such as those occurring with allergies, is required to develop successful intervention strategies and control respiratory disease in animals