Publications

A growing body of research suggests that perceived discrimination, in multiple societies, is a neglected but important predictor of increased risk of disease for a broad range of health status indicators. Several prior studies propose that discrimination is adversely related to increased cardiovascular disease risk. The studies by Hunte (Am J Epidemiol. 2011;173(11):1223-1231) and Lewis et al. (Am J Epidemiol. 2011;173(11):1232-1239) find that self-reported discrimination is associated with increased risk of adiposity for men and women. These studies highlight the potentially important role of discrimination as a risk factor for excess fat but also raise important research questions regarding the role of fat in cardiovascular disease and racial differences in these processes. More generally, they also provide an important reminder to epidemiologists and medical professionals that discrimination and other aspects of racism persist in contemporary society and that increased efforts are needed to document the extent to which they may have pathogenic consequences and to identify the most promising initiatives to reduce any observed negative effects. Equally important, these studies remind us that, although social stressors are difficult to measure accurately and comprehensively, understanding how multiple stressors combine over the life course to affect the risk of morbidity and mortality remains an important priority for concerted research attention.

RATIONALE

Idiopathic pulmonary fibrosis is a progressive, uniformly fatal interstitial lung disease. An acute exacerbation of idiopathic pulmonary fibrosis is an episode of acute respiratory worsening without an identifiable etiology. Occult viral infection has been proposed as a possible cause of acute exacerbation.

OBJECTIVES

To use unbiased genomics-based discovery methods to define the role of viruses in acute exacerbation of idiopathic pulmonary fibrosis.

METHODS

Bronchoalveolar lavage and serum from patients with acute exacerbation of idiopathic pulmonary fibrosis, stable disease, and acute lung injury were tested for viral nucleic acid using multiplex polymerase chain reaction, pan-viral microarray, and high-throughput cDNA sequencing.

MEASUREMENTS AND MAIN RESULTS

Four of forty-three patients with acute exacerbation of idiopathic pulmonary fibrosis had evidence of common respiratory viral infection (parainfluenza [n = 1], rhinovirus [n = 2], coronavirus [n = 1]); no viruses were detected in the bronchoalveolar lavage from stable patients. Pan-viral microarrays revealed additional evidence of viral infection (herpes simplex virus [n = 1], Epstein-Barr virus [n = 2], and torque teno virus [TTV] [n = 12]) in patients with acute exacerbation. TTV infection was significantly more common in patients with acute exacerbation than stable controls (P = 0.0003), but present in a similar percentage of acute lung injury controls. Deep sequencing of a subset of acute exacerbation cases confirmed the presence of TTV but did not identify additional viruses.

CONCLUSIONS

Viral infection was not detected in most cases of acute exacerbation of idiopathic pulmonary fibrosis. TTV was present in a significant minority of cases, and cases of acute lung injury; the clinical significance of this finding remains to be determined.