VIrises do not often have a positive effect, and infections generally do not lead to positive health effects. But during the pandemic, some doctors began to notice anecdotally that some people with cancer who became very ill from COVID-19 saw their tumors shrink or grow more slowly.
“We didn’t know if it was real because these patients were so sick,” said Dr. Ankit Bharat, chief of Thoracic Surgery at Northwestern University. “Was it because the immune system was so triggered by COVID-19 that it also started killing cancer cells? What was it?”
Bharat and his team decided to conduct a study to find out whether the apparent ‘benefit’ of COVID-19 for these cancer patients could teach them something about a possible new way to fight cancer – or if it was just a red herring. They published their findings on November 15 in the Journal of Clinical Research.
Using a combination of human cells and animal models, Bharat and his team discovered that in the presence of SARS-CoV-2, immune cells called monocytes act differently than normal. Normally, as part of the immune system, monocytes travel through the bloodstream and alert other immune cells to the presence of foreign cells or pathogens; some monocytes can attract cancer-killing immune cells to tumors, but others are not as effective at doing so. That’s because cancer cells can in some cases co-opt monocytes — “like a demon summoning forces,” says Bharat — and form an immune wall that protects the tumor from detection and attack by additional immune defense mechanisms.
But during a COVID-19 infection, SARS-CoV-2 attaches to these monocytes, allowing them to resume their original task: defending the body against cancer. “They look the same and are still recruited to the tumor sites, but instead of protecting the cancer cells, they start bringing specific natural killer cells (the body’s main cells that kill cancer) to these tumor sites,” says Bharat. . “So where previously the cancer brainwashed the monocytes to protect the cancer, now the virus helps them attack the cancer.”
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It’s a potentially powerful turnaround that – if confirmed by human studies – could provide a new way to control cancer. By analyzing the receptor on the monocytes to which the COVID-19 virus attached, Bharat found a compound that is not currently used to treat any disease, but which closely mimics the COVID-19 virus in the way it binds to the monocyte. to induce the cell’s transformation into a cancer-fighting cell. “We can use a drug to produce the same effect as the RNA of the COVID-19 virus,” he says. “By manipulating that pathway through the drug, we may be able to help patients with many different types of cancer, especially those with stage 4 cancer.”
In animal tests, the compound, called muramyl dipeptide (MDP), reduced tumors by 60% to 70% in mice with human cancers, including breast, colon, lung and melanoma.
More studies are needed to confirm whether the cells have the same cancer-fighting effect in humans, but there are promising indications. These transformed, cancer-causing monocytes, called inducible non-classical monocytes, are rare compared to other types of monocytes but tend to proliferate when inflammation occurs, such as during a COVID-19 infection. Transplant surgeons have previously identified them in people who have undergone lung and spleen transplants, and Bharat is conducting additional research to understand why the transplant process and COVID-19 infections – both of which activate the immune system – trigger the specific change in the monocytes. Interestingly, the transformation does not occur in all RNA-based viruses; Bharat tested influenza and parainfluenza, which are also RNA viruses, and did not see the same population of cancer-fighting monocytes emerge.
Another intriguing part of the equation, says Bharat, is that this pathway is independent of the T-cell immune treatments that are now becoming a major part of cancer therapy, in which doctors increase the population of T-cells that can recognize cancer cells and to attack. They can be effective, but generally only work for a while, as cancers quickly find ways to evade the T cells and become resistant to the therapies.
In contrast, the virus-induced changes in monocytes are not dependent on T cells. Bharat tested the approach in mice genetically bred to lack T cells and still saw a strong effect on tumors in these animals through the monocytes. That means the monocytes can help boost the body’s response to immunotherapy – and its ability to fight tumors. Much more research is needed before the finding leads to treatments. But “this approach could potentially be used to promote regression,” he says.