STAT has an article discussing some emerging details of unique ways that the SARS-CoV-2 virus interacts with the immune system and hijacks host cells that may explain some of the severe inflammatory complications that are often the life-threatening events in COVID-19 disease.
The Cell article highlights how the virus seems to act differently towards two aspects of human immune response to viruses -- the first involves interferons (IF) that work by recognizing the virus and controlling/slowing its replication, and the second involves chemokines that recruits white blood cells to the area to actively fight the virus, which is what produces inflammatory responses. Many viruses have proteins that suppress both of these activities; this article highlights evidence that SARS-CoV-2 seems adept at reducing interferon expression, allowing the virus to quickly replicate (supported also by bioRxiv model), yet does not reduce the chemokine, so does not suppress inflammatory response.
This is interesting since it appears the major severity of the disease in advanced cases involves overactive and out of control inflammatory response, blocking the lungs' ability to oxygenate blood, leading to extreme clotting problems that can produce embolisms, or even in some cases when getting to the brain causing inflammation of the brain.
There is still a lot to learn about the specific mechanism by which the virus works, but these kinds of insights are key to find the right targeted therapeutic strategies for prevention and treatment of mild disease to prevent progression, as well as treating the advanced cases with severe symptoms.
It is exciting to see the scientific community working fast to find insights that will hopefully lead to prevention and treatment strategies in much faster time frames than is typical for other diseases.