SARS-CoV-2 pneumonia triggers lung squamous p16-related dysplasia? A preliminary necroscopic investigation

There is still today little scientific evidence that COVID-19, the disease caused by the SARS-CoV-2 virus, could be responsible for causing long-term effects. However, histological changes in the lungs of deceased people infected by SARS-CoV-2 were seen to have occurred, resulting in areas of squamous metaplasia, atypical pneumocytes and a proliferation of fibroblasts. Herein, we report two case studies of subjects who had previously contracted the SARS-CoV-2 infection and later died of acute pneumonia. The two corpses subsequently underwent complete autopsies, histological examinations and immunohistochemical analysis. The analysis showed up areas of squamous metaplasia and dysplasia, as well as a high immunohistochemical expression of the protein p16 in the lungs. Given the fact that p16 is codified on the INK4/ARF locus, which is one of the genomic areas most frequently affected by human tumors, the loss of its function can bring about an uncontrollable multiplication of cells. Therefore, it cannot be excluded that the pulmonary infection caused by the SARS-CoV-2 virus may have an inductive neoplastic role. In other words, the carcinogenic mechanism could be linked to either the alteration of onco-suppressive genes or oncogenes or to the oxidative stress brought about by the infection itself. Therefore, the aim of our present study is to investigate the possible role of the SARS-CoV-2 virus in association with mutagenesis and cancerogenesis.