Respiratory syncytial virus (RSV) is the most common viral cause of childhood acute lower
respiratory tract infections. It is estimated that
RSV infections result in more than 100,000 deaths annually worldwide. Bovine RSV is a cause of enzootic
pneumonia in young dairy calves and summer
pneumonia in nursing beef calves. Furthermore, bovine RSV plays a significant role in
bovine respiratory disease complex, the most prevalent cause of morbidity and mortality among feedlot cattle.
Infection of calves with bovine RSV shares features in common with
RSV infection in children, such as an age-dependent susceptibility. In addition, comparable microscopic lesions consisting of bronchiolar neutrophilic infiltrates, epithelial cell
necrosis, and syncytial cell formation are observed. Further, our studies have shown an upregulation of pro-inflammatory mediators in RSV-infected calves, including
IL-12p40 and CXCL8 (IL-8). This finding is consistent with increased levels of
IL-8 observed in children with RSV
bronchiolitis. Since rodents lack
IL-8, neonatal calves can be useful for studies of
IL-8 regulation in response to
RSV infection. We have recently found that
vitamin D in milk replacer diets can be manipulated to produce calves differing in circulating
25-hydroxyvitamin D3. The results to date indicate that although the
vitamin D intracrine pathway is activated during
RSV infection, pro-inflammatory mediators frequently inhibited by the
vitamin D intacrine pathway in vitro are, in fact, upregulated or unaffected in lungs of infected calves. This review will summarize available data that provide parallels between bovine
RSV infection in neonatal calves and human RSV in infants.