Altered Pathogenesis of Porcine Respiratory Coronavirus in Pigs due to Immunosuppressive Effects of Dexamethasone: Implications for Corticosteroid Use in Treatment of Severe Acute Respiratory Syndrome Coronavirus

Abstract

The pathogenesis and optimal treatments for severe acute respiratory syndrome (SARS) are unclear, although corticosteroids were used to reduce lung and systemic inflammation. Because the pulmonary pathology of porcine respiratory coronavirus (PRCV) in pigs resembles SARS, we used PRCV as a model to clarify the effects of the corticosteroid dexamethasone (

Porcine reproductive and respiratory syndrome virus modifies innate immunity and alters disease outcome in pigs subsequently infected with porcine respiratory coronavirus: implications for respiratory viral co-infections

“…The ISU-1 strain of PRCV was plaque purified twice and passaged 14 times in swine testicle (ST) cells. Virus titers were assayed by plaque assays as plaque-forming units (PFU/ml), as described previously (Jung et al , 2007). …”

“…All inoculation procedures were performed using aseptic techniques. After PRRSV inoculation, we monitored clinical signs and body weight gains every other day as previously described (Jung et al , 2007). At prior [post-inoculation day (PID) -2], early (PID 2 and 4), middle (PID 8 and 10), and late (PID 14 and 21) stages of PRCV infection, 5 to 8 pigs per group were euthanized by electrocution as recommended by the American Veterinary Medical Association (AVMA) panel report (2000).…”

“…PRCV causes mainly upper and lower respiratory tract disease, infects type 1 and 2 pneumocytes, and induces acute pulmonary cell damage (Cox et al , 1990; Halbur et al , 1993; Jabrane et al , 1994; Jung et al , 2007). Even up to 10 days after PRCV infection of lung tissues, the virus simultaneously induces inflammatory (cell necrotizing) and proliferative (alveolar septa thickening) pneumonia, i.e., chronic-active bronchointerstitial pneumonia (Jung et al , 2007).…”

“…PRCV causes mainly upper and lower respiratory tract disease, infects type 1 and 2 pneumocytes, and induces acute pulmonary cell damage (Cox et al , 1990; Halbur et al , 1993; Jabrane et al , 1994; Jung et al , 2007). Even up to 10 days after PRCV infection of lung tissues, the virus simultaneously induces inflammatory (cell necrotizing) and proliferative (alveolar septa thickening) pneumonia, i.e., chronic-active bronchointerstitial pneumonia (Jung et al , 2007). PRCV also stimulates production of IFN-α in lung and thus promotes local innate immune responses, similar to that seen in SARS in humans (Charley et al , 2006; Frieman et al , 2008; Thiel & Weber, 2008; Van Reeth et al , 1999; Zhang et al , 2008).…”

Lung Cell Tropism and Inflammatory Cytokine-Profile of Porcine Respiratory Coronavirus Infection

“…This suggests that massive production of proinflammatory cytokines, or perhaps other factors in addition to cytokines are necessary for the development of clinical symptoms. PRCV infection in pigs has previously been suggested as a good model for studying the effect of corticosteroids on severe acute respiratory syndrome coronavirus (SARS-CoV) infection in humans [46]. Chen and Subbarao have done an extensive summary on currently available knowledge of SARS immunobiology [47].…”