Background
Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with a mean survival rate of less than 3 years. The prevalence of IPF is estimated at up to 29 cases per 100,000, with the incidence and associated mortality currently increasing.[1,2] Many risk factors have been implicated in the etiology of IPF including inhaled toxins, smoking and infectious disease.[3,4] However, the specific mechanisms underlying IPF pathogenesis or disease progression are unknown.
Extensive research has demonstrated a role for a number of viruses in initiation and progression of clinical disease in IPF. Previous research has demonstrated a role of viruses in initiation and progression of clinical disease in IPF.[5–9] Previously, we demonstrated the presence of parainfluenza, RSV, rhinovirus and coronavirus in nasopharyngeal (NPL) and bronchoalveolar lavage (BAL) fluid from IPF patients.[4] However, we did not investigate the impact of these viruses on pulmonary function in IPF patients. The similarities in clinical and radiologic presentation between pneumonitis related to viral infection and acute exacerbation of IPF (AE-IPF) in patients illustrates the key role of viruses in the pathogenesis of IPF.[10]
More recently, a role for bacterial infection has been described in the pathogenesis of IPF. Studies have demonstrated that IPF patients have an increased bacterial load in BAL fluid compared with healthy individuals or COPD patients.
