Abstract
COVID-19, caused by SARS-CoV-2, is a primarily pulmonary disease that can affect several organs, directly or indirectly. To date, there are many questions about the different pathological mechanisms. Here, we generate an approach to identify the cellular-level tropism of SARS-CoV-2 using human proteomics, virus-host interactions, and enrichment analysis. Through a network-based approach, the molecular context was visualized and analyzed. This procedure was also performed for SARS-CoV-1. We obtained proteomes and interactomes from 145 different cells corresponding to 57 different tissues. Not all cells had proteins such as ACE2 or TMPRSS2 (among others), so they were discarded. Of the remaining cells, a gradient of susceptibility to infection was observed. In addition, proteins associated with the coagulation cascade that can be directly or indirectly sequestered by viral proteins were identified. We have identified 55 potential cells that can be "cracked" with different susceptibilities. One of the main results being pneumocytes, as well as heart, kidney, liver, or small intestine. We also report how the coagulation cascade can be affected by SASR-CoV-2 infection. These results help us to explain the molecular context and provide elements for possible treatments in the current situation.