TABLE 1

Summary of studies linking viruses with the pathogenesis, progression and acute exacerbation of idiopathic pulmonary fibrosis (IPF)

VirusMain conclusions[Ref.]
HHVEBV detected in serum of 12 out of 13 subjects with IPF but not in patients with other forms of ILD[22]
MHV-68 triggers an exaggerated fibrotic response in mice[23]
Increased incidence of EBV in BAL and lung biopsies of IPF subjects compared to controls[24, 25]
EBV detected in BAL of two out of 43 AE-IPF subjects[26]
CMV detected in BAL of two out of 43 AE-IPF subjects[27]
A total of 38% of AE-IPF subjects exhibited evidence of CMV infection[28]
HHV detected in nasopharyngeal swabs of 15 out of 30 AE-IPF subjects and four out of 30 individuals with stable IPF[29]
TTVTTV detected in BAL of 12 out of 43 AE-IPF subjects[26]
No evidence of TTV in BAL of stable IPF subjects[30]
Increased mortality in IPF subjects with presence of TTV-DNA in serum compared to IPF subjects with no TTV-DNA
Influenza AInfluenza A detected in nasopharyngeal swabs of 12 out of 30 AE-IPF subjects but not in individuals with stable IPF[29]
A case of AE-IPF was reported following pandemic influenza A vaccination[31]

HHV: human herpes virus; TTV: torque teno virus; EBV: Epstein–Barr virus; ILD: interstitial lung disease; MHV-68: murine γherpes virus-68; BAL: bronchoalveolar lavage; AE-IPF: acute exacerbation of IPF; CMV: cytomegalovirus.