Table 1. A synopsis of studies linking viruses with the pathogenesis, progression and (acute) exacerbation of idiopathic pulmonary fibrosis (IPF)

Virus	Major study findings	Comment
HCV	28% of an IPF cohort had evidence of prior HCV compared with 3.6% of controls [8]	The lack of a coherent signal across studies suggests that HCV is unlikely to be an important trigger for the development of IPF
	Incidence of IPF higher in cohort of HCV positive individuals compared to cohort with HBV [9]
	No association between IPF and HCV [10]
	Association of HCV with a range of non-fibrotic respiratory conditions [11]
TTV	Lower survival rate in IPF patients with presence of TTV-DNA in serum compared to IPF with no TTV-DNA [12]	Link to pathogenesis unclear. May cause progression of disease or be linked to the development of acute exacerbations
TTV	Detected in BAL during IPF exacerbation and in individuals with acute lung injury [13]
HHV	12 out of 13 IPF patients seropositive for EBV [14]	Some conflicting evidence but potential role of HHVs as a co-factor in the initiation and progression of IPF
	Increased EBV in lung biopsy samples and BAL from individuals with IPF compared with controls [15–17]
	At least one HHV detected in 97% of IPF patients compared with 36% controls [18, 19].
	MHV triggers and enhances fibrotic response in mice [20–23]

HCV: hepatitis C virus; TTV: transfusion transmitted virus; HHV: human herpes virus; HBV: hepatitis B virus; BAL: bronchoalveolar lavage; EBV: Epstein�–Barr virus; MHV: murine herpes virus.