Idiopathic fibrosing alveolitis is still not well understood. The following etiological factors are currently being discussed: Viruses that are "undetectable" or "slow," such as the hepatitis C virus and the human immunodeficiency virus, are the most common. Viruses are thought to play a dual role in the progression of idiopathic fibrosing alveolitis: they are the primary cause of lung tissue deterioration, and the virus then multiplies in the already damaged tissues, leading to disease progression.
Viruses have also been shown to interact with genes that regulate cell growth, resulting in increased collagen formation and fibro-oocyte production. In addition, viruses can exacerbate pre-existing chronic inflammation. Idiopathic fibrosing alveolitis has been linked to extensive professional contact with metal and wood dust, brass, lead, steel, and various types of inorganic dust, such as asbestos and silicon. It's not impossible that aggressive etiological elements contributed to the aetiology.
It is important to note, however, that these workplace conditions cause pneumoconiosis and, in the case of idiopathic fibrosing alveolitis, almost certainly contribute to its development. The fact that family members can become ill emphasises the significance of hereditary predisposition. Hereditary polymorphisms in genes encoding proteins involved in antigen processing and presentation to T cells are thought to underpin the genetic predisposition to idiopathic fibrosing alveolitis. The major pathophysiological features of idiopathic fibrosing alveolitis are broad intermittent lung tissue inflammation and the subsequent development of an intensive and widespread fibrotic process. Pulmonary interstitial tissue is a type I collagen-based connective tissue matrix found in the alveolar wall that is bordered by epithelial and endothelial basal membranes. Both sides of the membrane are filled with alveolar epithelium, which is common for two adjacent alveoli.