However, even after the exclusion of any identifi able and treatable factor(s) inducing IPF exacerbations, the most important etiologic hypothesis remains that of a clinically occult infection that precipitates an already UIP-scarred lung into DAD [6] . For several reasons, viruses are the best etiologic candidates: (a) Epstein-Barr, cytomegalovirus, hepatitis C, herpes simplex, parvovirus B19, torque teno, and especially herpes viruses 7 and 8 have been implicated in IPF pathogenesis [40] [41] [42] ; (b) fl ulike illness heralds the onset of exacerbations, and IPF mortality seems to peak in winter time and coincides with the peak of viral respira tory infections [43] ; (c) in the mice pulmonary fi brosis experimental model, gamma herpesvirus induces exacer ba tions [44] as well as other viruses in vivo [45] ; and (d) latent lung viral infections may reactivate under immuno suppression commonly used by clinicians [41] . Th erefore, in IPF, viruses may act as both initiators and exacerbators because of their formidable ability to induce ARDS [46] . Besides viruses, microbials in traction bronchiectases/ bronchiolectases are equally strong candidates. Bronchiec tases are among the most common of the whole spectrum of lesions that characterize the architectural distortion in IPF. Interleukin-8, neutrophils, and alphadefensins are increased or activated in stable or exacerbated patients with IPF [47, 48] and possibly play a role in triggering ARDS. In addition, immunosuppressive treatment certainly increases suscep ti bility to microbials.