Fig. 2.

Gu’s hypothesis, concerning SARS-CoV infection⁽¹⁴⁾. A similar scheme may be considered with the purpose to explain the pathogenesis of SARS-CoV-2. The SARS-CoV infects the human body through the respiratory tract, entering the epithelial cells of the trachea, bronchi, bronchioles and lungs. In this context, the virus also colonises resident, infiltrating and circulating immune cells. Then, the virus disseminates to all human organs, being carried by the infected circulating immune cells and spread to different types of cells in other organs. The immune cells of the spleen, peripheral and central lymph nodes, other lymphoid tissues are colonised and damaged by the virus. Furthermore, the mucosa of the intestine, the epithelium of the renal distal tubules, the neurons of the brain and the macrophages in different organs are also involved. According to this hypothesis, it may be assumed that infected circulating immune cells spread to the mucosa-associated lymphoid tissue (MALT) and bronchus-associated lymphoid tissue (BALT) The immune defence is significantly impaired and infected patients may develop pneumonia with different degrees of severity and experiment a rapid deterioration of clinical conditions. Aged subjects with chronic diseases have often a compromised immune function, generally develop more severe clinical pictures and present a more elevated mortality in comparison with healthy subjects. The severity of the immune cell damage more than the extent of the lesions detectable in the lungs suggests the patient’s immune status, and his lymphocyte count probably represents the main predictor of his clinical evolution. Viral load also may exert a crucial impact on the strength and efficacy of the patient’s immune response. The possible action of fat-soluble vitamins in improving immune response activity is indicated. ARDS, acute respiratory distress syndrome.