How SARS-CoV-2 disables our cells’ alarm system, and what we can do about it
Drrrrrrrrrrrriiiinggggggggggggg!
Much like the jolt you get from your morning alarm, the innate immune system alerts the cells in your body to an invading threat. When you breathe in a respiratory virus like SARS-Coronavirus-2, the cells in the upper airways of your nose and throat are the first to become infected. As the virus invades one or more of these cells, it will trigger an innate immune response. Once triggered, a cell can use messages, like a protein called interferon, to notify its neighbors that there is an eminent threat. Not only do these messages warn nearby cells of the intruder, helping them to mount a defense, but they also relay essential information to the heavy hitters of the immune system, the B cells and T cells, to take over and either trap or kill the invading coronavirus.
The villainous virus driving the ongoing pandemic, SARS-CoV-2, however, is particularly good at blocking communication between an infected cell and its neighbors. Throughout its ongoing spread and evolution, the virus has accumulated changes that allow it to suppress innate immunity. One way that the virus accomplishes this is by suppressing or delaying the expression of important antiviral messengers like interferon. This important protein messenger gets sent from cell to cell and activates the expression of genes that help to limit a virus’ replication and spread. Thanks in part to its disruption of interferon-based cell communication, SARS-CoV-2 can remain undetected within the cells of your respiratory tract for enough time to allow the virus to reproduce to high levels and spread throughout the body. This causes disease and, in some cases, the delayed expression of that important messenger, interferon, can cause severe inflammation, and even death.
But there is hope! Antiviral drugs, especially when given in the early stages of an infection, can control the spread of the virus by blocking its ability to disable our cellular alarm systems. When SARS-CoV-2 is kept in check by innate immunity, the virus will be less able to spread throughout the body, leading to less disease! With the important changes that variants like Omicron have accumulated, it’s particularly important to think about how to design drugs that will target parts of the virus that are not changing, in order to build an arsenal of effective drugs to treat all variants of this virus.
Olivia Kern is a second year PhD student studying how emerging variants of SARS-CoV-2 outsmart the body’s early defenses. She is particularly interested in connecting the tactics that the virus uses when it infects our lung cells to disease severity, in order to develop drugs and vaccines that combat all coronaviruses.