Study details and key findings
For the study, researchers used a unique mouse model of metastatic breast cancer, which included dormant disseminated cancer cells (DCCs), or cells that break off from a primary tumor and spread to other organs. The mice overexpressed a gene related to the human gene HER2, which produces a protein that causes breast cancer cells to reproduce rapidly.
According to James DeGregori, a biochemistry professor at the University of Colorado School of Medicine and one of the study’s senior authors, the mouse model was designed to show what human patients with breast cancer may experience over several years or even decades.
After exposing the mice to either influenza viruses or SARS-CoV-2, the COVID-19 virus, the researchers found that the metastatic burden in the mice increased significantly, between 100-fold and 1000-fold. The researchers also found that viral infection caused dormant cancer cells to evolve into a previously unrecognized hybrid state, which suggests that the infection somehow promoted the activation of cancer cells.
Through a molecular analysis, the researchers found that the dormant DCCs were reactivated by interleukin-6 (IL-6), an inflammatory protein released by immune cells in response to injuries or infection. According to STAT, other studies have linked inflammation, as well as IL-6 specifically, to the formation of metastatic lesions.
In addition, the researchers found that CD4 cells, a type of immune T cells, seemed to suppress anti-tumor activity after viral infection, which made it harder to eliminate cancer cells.
“Instead of the immune system actively eliminating the cancer cells, it protects them from immune elimination,” DeGregori said. “We need to better understand this mechanism of immune suppression so that perhaps we can reverse it and allow the immune system to better control the cancer.”