Hepatitis C virus enhances incidence of idiopathic pulmonary fibrosis

Arase, Yasuji; Suzuki, Fumitaka; Suzuki, Yoshiyuki; Akuta, Norio; Kobayashi, Masahiro; Kawamura, Yusuke; Yatsuji, Hiromi; Sezaki, Hitomi; Hosaka, Tetsuya; Hirakawa, Miharu; Saito, Satoshi; Ikeda, Kenji; Kumada, Hiromitsu

doi:10.3748/wjg.14.5880

Cited by 73 publications

(47 citation statements)

References 34 publications

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“…A Japanese case-control study relying on self-reported diagnosis of HCV infection also did not find a significant association between HCV infection and the risk of developing IPF [57]. More recently, among more than 6,000 Japanese HCVinfected patients, 15 developed IPF during a mean followup of 8 years, whereas IPF was not diagnosed in any of more than 2,000 hepatitis B virus-infected patients followed for a mean of 6.3 years [58]. In particular, HCV patients aged ≥55 years, with ≥20 pack-years of smoking and who had liver cirrhosis were at increased risk of developing IPF.…”

Section: Hepatitis C Virusmentioning

confidence: 89%

Idiopathic Pulmonary Fibrosis—an Epidemiological and Pathological Review

Borchers

Chang²,

Keen

et al. 2010

Clinic Rev Allerg Immunol

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Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease (ILD) affecting the pulmonary interstitium. Other forms of interstitial lung disease exist, and in some cases, an environmental etiology can be delineated. The diagnosis of IPF is typically established by high-resolution CT scan. IPF tends to have a worse prognosis than other forms of ILD. Familial cases of IPF also exist, suggesting a genetic predisposition; telomerase mutations have been observed to occur in familial IPF, which may also explain the increase in IPF with advancing age. Alveolar epithelial cells are believed to be the primary target of environmental agents that have been putatively associated with IPF. These agents may include toxins, viruses, or the autoantibodies found in collagen vascular diseases. The mechanism of disease is still unclear in IPF, but aberrations in fibroblast differentiation, activation, and proliferation may play a role. Epithelial-mesenchymal transition may also be an important factor in the pathogenesis, as it may lead to accumulation of fibroblasts in the lung and a disruption of normal tissue structure. Abnormalities in other components of the immune system, including T cells, B cells, and dendritic cells, as well as the development of ectopic lymphoid tissue, have also been observed to occur in IPF and may play a role in the stimulation of fibrosis that is a hallmark of the disease. It is becoming increasingly clear that the pathogenesis of IPF is indeed a complex and convoluted process that involves numerous cell types and humoral factors.

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Section: Hepatitis C Virusmentioning

confidence: 89%

Idiopathic Pulmonary Fibrosis—an Epidemiological and Pathological Review

Borchers

Chang²,

Keen

et al. 2010

Clinic Rev Allerg Immunol

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“…In a Japanese study, which contained 66 subjects with IPF and 9646 controls, UEDA et al [8] found that 28.8% of IPF subjects, but only 3.66% of controls, had evidence of prior HCV infection. ARASE et al [9] addressed the same question from the opposite direction. They studied a cohort of 6150 patients with HCV and a cohort of 2050 patients with Hepatitis B (HBV).…”

Section: Infection and The Pathogenesis Of Ipfmentioning

confidence: 93%

“…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 [ subjects when compared to controls [15][16][17]25]. Whilst EBV has been the most frequently studied of the HHVs, TANG et al [18] looked more broadly at a range of HHV family members and found evidence of past infection with at least one HHV in 97% of patients with IPF compared to only 36% of healthy controls.…”

Section: Virusmentioning

confidence: 99%

The role of infection in the pathogenesis of idiopathic pulmonary fibrosis

Molyneaux

Maher

2013

European Respiratory Review

147

112

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Idiopathic pulmonary fibrosis (IPF) is a progressive, and invariably fatal, condition that is believed to arise in genetically susceptible individuals as a consequence of an aberrant wound-healing response following repetitive alveolar injury. The exact triggers, which initiate the fibrotic process, remain unknown. Infectious agents, including both viruses and bacteria, have the capacity to cause alveolarepithelial cell injury and apoptosis. Relatively few studies have examined the role of infection in IPF. Those that have, point to viruses playing a key role as cofactors in the initiation and progression of IPF. There is also some evidence to suggest that viral infection may be responsible for a proportion of acute exacerbations of IPF. The role played by bacteria in the pathogenesis of IPF is less clear cut. Studies from other respiratory diseases suggest that alterations in the lung microbiome are associated with disease and that these changes influence disease behaviour. Emerging molecular microbiological techniques are making the study of microbial communities in the lung easier. It is hoped that by combining such techniques with the careful longitudinal phenotyping of patients with IPF, it will be possible to elucidate the role played by bacteria and viruses in the pathogenesis of the disease. If infection plays a causal role in IPF then it is possible that therapeutic strategies, utilising currently available antiviral or antibiotic drugs, may be effective in modifying the course of this devastating condition.@ERSpublications Understanding viral and bacterial involvement in IPF could help development of novel therapeutic approaches

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“…A major concern, that has not been fully addressed, is the possibility that enhanced levels of some of these biomarkers can be found in IIPs as well as in malignancies, while these diseases may very well coincide. For example, an increased incidence of IPF has been reported in patients with hepatitis C virus (HCV) infection [73][74]. Arase et al reported increased levels of KL-6 one year before clinical onset of IPF in HCV patients [75].…”

Section: Discussionmentioning

confidence: 99%