Idiopathic fibrosing alveolitis still hasn't been properly identified. The following etiological factors are now being debated:The most prevalent viruses are those that are "undetectable" or "slow," such as the hepatitis C virus and the human immunodeficiency virus. Viruses are assumed to play a dual function in the development of idiopathic fibrosing alveolitis: they are the primary cause of lung tissue deterioration, and the virus subsequently multiplies in the already injured tissues, leading to disease progression. Viruses have also been shown to interact with genes that drive cell growth, increasing collagen formation and fibro-oocyte production. Viruses can also worsen pre-existing chronic inflammation. Extensive professional contact with metal and wood dust, brass, lead, steel, and various types of inorganic dust, such as asbestos and silicon, has been linked to idiopathic fibrosing alveolitis. It's hardly impossible that aggressive etiological elements played a role in the etiology. It's essential to mention, though, that these workplace conditions cause pneumoconiosis and, in the case of idiopathic fibrosing alveolitis, are almost certainly help to build up. The fact that family members can get sick underscores the importance of hereditary predisposition. The genetic predisposition to idiopathic fibrosing alveolitis is assumed to be based on hereditary polymorphisms of genes encoding proteins involved in antigen processing and presentation to T cells. In idiopathic fibrosing alveolitis, the major pathophysiological features are broad intermittent lung tissue inflammation and the subsequent development of an intensive and broad fibrotic process. Pulmonary interstitial tissue is a type I collagen-based connective tissue matrix that is bordered by epithelial and endothelial basal membranes and is found in the alveolar wall. The alveolar epithelium fills both sides of the membrane, which is common for two adjacent alveoli.