Disease relevance of PI3

• Killing of Staphylococcus epidermidis by AM was determined on days 1-4 post-infection (p.i.) PI3 virus-infected AM killed significantly fewer bacteria on day 4 p.i. compared to uninfected controls (12.1 +/- 1.3% infected vs. 52.7 +/- 7.2% controls, P less than or equal to 0.05) [1].
• The antibodies were tested for cross-reactivity with bovine PI3 virus, Sendai virus, and simian virus 5 (SV5) [2].
• An enzyme linked immunosorbent assay (ELISA) was applied to the detection of serum antibodies against infectious bovine rhinotracheitis (IBR), parainfluenza-3 (PI3), adenovirus type 3 (adeno 3) and bovine respiratory syncytial (BRS) viruses [3].
• The effect of the administration of recombinant human interferon on the severity of clinical disease and the extent of pneumonic lesions in calves infected experimentally with bovine parainfluenza 3 (PI3) virus was studied in two experiments [4].
• Pulmonary lavage samples were collected from 90- to 130-day-old calves before and 6 days after aerosol inoculation with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI3) virus [5].

High impact information on PI3

• Studies with genistein and PP2 showed that the nonreceptor tyrosine kinase, Src, is an upstream stimulator of the PI3 kinase-Akt pathway in this paradigm [6].
• PI-3 modified the twin signals of calcium and protein kinase C in alveolar macrophages [7].
• PI-3 did not trigger O2- generation before inhibition, whereas influenza triggered O2- generation before desensitization of ligand-initiated respiratory burst [7].
• Bovine parainfluenza-3 (PI-3) virus inhibits oxygen-dependent bacterial killing by phagocytes, a key pulmonary defense, thus predisposing the host to intrapulmonary bacterial superinfection [7].
• These effects further distinguish bovine PI-3 from human influenza, which triggers mobilization of cell-associated calcium and inhibits calcium mobilization activated by physiologic ligands [7].

Chemical compound and disease context of PI3

• A luminol-amplified chemiluminescence (CL) assay was used to evaluate the effect of levamisole on the metabolic activity of pulmonary alveolar macrophages (PAM) from parainfluenza-3 (PI-3) and infectious bovine rhinotracheitis (IBR) virus-infected calves [8].

Biological context of PI3

• The ELISA compared favorably with the virus neutralization test for detecting serologic responses to IBR, BRS, and adeno 3 viruses or with the hemagglutination inhibition test for PI3 virus [3].
• Peripheral blood mononuclear cells (PBMC) from normal cattle of different ages and from specific pathogen-free (SPF) calves, 2 to 4 weeks old, were cultured with bovine herpes virus type 1 (BHV1), parainfluenza-3 virus (PI3) and phytohaemagglutinin (PHA) [9].
• Immunospecific production of IFN-gamma provides a simple method for monitoring cell-mediated immunity in BHV1- and PI3 virus-infected calves and can be used for evaluating the efficacy of vaccines against these viruses [10].
• Inhibition of Ca-independent, PS/DG-dependent kinase activity and inhibition of O2- generation by PI-3 occurred at a similar viral dose and time frame, suggesting a role for this kinase in activating the respiratory burst [7].
• Activation of the phosphatidylinositol-3-phosphate (PI-3) kinase pathway by sCD40L, as determined by the measurement of Akt phosphorylation, was not detected [11].

Anatomical context of PI3

• However, ROS did inhibit the Phosphoinositide 3-kinase (PI3) activity when oocytes mature without EGF [12].
• Cases were positively associated with the presence of neutrophils and Pasteurella multocida in BAL fluid and negatively associated with PI3 virus and PhIA seroconversion [13].
• Recovery of infective PI-3 virus from infected peritoneal and lung macrophages extended over 4 to 8 days, respectively [14].
• A similar relationship to blood BHBA concentration was not observed with the lymphocyte proliferation to BVDV, PI-3, or BHV-1 [15].
• Infective virus could not be recovered from PMN, RBC, lymphocytes, or monocytes for more than 24 hours after PI-3 infection [14].

Associations of PI3 with chemical compounds

• A significant (P less than or equal to 0.05) increase in the percentage of phosphatidylethanolamine to 18.1 +/- 2.2% and 17.8 +/- 4.5% developed in calves inoculated with BHV-1 and PI3 virus, respectively [5].
• Infection with either of the 2 viruses caused a significant (P less than or equal to 0.05) decrease in the percentage of phosphatidylcholine to 66.0 +/- 8.0% and 65.1 +/- 10.8% in the calves inoculated with BHV-1 and PI3 virus, respectively [5].
• Feeder calves were vaccinated with modified live virus (MLV) bovine parainfluenza-3 (PI-3) vaccines by the nasal and parenteral routes [16].
• Calcium ionophore A23187 (5 X 10(-6) M)-induced release (% total, means +/- SEM) was: 51.53 +/- 3.05, 50.02 +/- 2.70, 83.91 +/- 4.09, 75.21 +/- 4.51 and 70.59 +/- 6.91 for control, LEV, PI-3, LEV + PI-3 and P. haemolytica groups, respectively [17].

Other interactions of PI3

• However, inactivated PI3 virus failed to induce IFN in PBMC cultures from normal cattle, but approximately half of the animals, mostly calves, produced IFN-gamma spontaneously in 48 h cultures in the absence of added antigen [9].

Analytical, diagnostic and therapeutic context of PI3

• Primary cultures of bovine AM obtained by bronchoalveolar lavage of normal cattle were infected in vitro with parainfluenza-3 (PI3 virus) virus [1].
• After the second vaccination serum antibodies to PI3 virus were detected in all four vaccinated calves, but not in the control animals [18].
• Inoculation of calves with 3.2 x 10(6) median cell culture infective doses (CCID50) of either virulent (SF-4) virus or a modified strain of PI-3 virus, or with 2.0 x 10(8) CCID50 of SF-4 virus, stimulated development of both serum antibody and nasal secretion (NS) antibody [19].
• Western blot analysis of ovine PI-3 virus using homologous serum produced 7 bands ranging in MW from 12 kD to 190 kD described for the first time in this paper [20].
• Epidemiology, pathogenesis, laboratory diagnosis, and important properties in infectious bovine rhinotracheitis (IBR), parainfluenza-3 (PI-3), and bovine respiratory coronavirus (BRCV) are described in this article [21].

References