Treatment & Immune Response
Immune Responses to COVID-19
Our bodies have two types of immune responses: innate and adaptive. The innate immune response is rapid, non-specific, and triggers the adaptive immune response. In turn, the adaptive immune response identifies particular pathogens, creates antibodies to attack those pathogens, and provides lasting immunity to the specific pathogens. COVID-19 treatments work by mimicking and bolstering these evolved immune response mechanisms.
Innate Immune Response
The innate immune response is triggered when any pathogen is detected. This response is performed by three types of white blood cells: dendritic cells, mast cells, and phagocytes.
Dendritic cells are common in the lungs, nose, stomach, and skin so they are usually the first white blood cells to detect a pathogen. These cells trigger the adaptive immune system by presenting pathogens to B-cells and T-cells, which are also specialized types of white blood cells that produce antibody proteins. As this is ongoing, mast cells release histamine, which causes blood vessels to expand and recruit other white blood cells to the region(s) of infection. Regions of infection will subsequently become inflamed, and if large areas of the body become inflamed, it may cause a fever. Phagocytes are large white blood cells that envelope and destroy pathogens and dead host cells.
Adaptive Immune Response
The adaptive immune response is triggered by the innate immune response and is performed by four types of white blood cells: helper T-cells, killer T-cells (also called cytotoxic T-cells), plasma B-cells, and memory B-cells.
When a SARS-CoV-2 virus is presented to a T-cell, it identifies the spike protein. When the same spike protein is detected by a helper T-cell, it will release specialized cytokine molecules, triggering inflammation. When helper T-cells or mast cells cause inflammation, heat shock proteins on killer T-cells are activated, allowing the killer T-cells to ‘stick’ to the infected areas. When a killer T-cell detects a virus, it can release cytotoxic compounds that destroy its target, or it may bind and destroy a cell infected with the virus.
When a SARS-CoV-2 spike protein is presented to a B-cell, the B-cell will create specialized antibodies that can bind to the spike protein. Plasma B-cells circulate throughout the body and release antibodies to bind to spike proteins when a virus is detected. After the infection is over, the plasma B-cells will no longer produce these antibodies. Memory B-cells and their antibodies remain in the host long after infection. When the host is reinfected with the same virus, the memory B-cells will quickly and efficiently detect the spike protein and trigger the adaptive immune response immediately. This usually results in the pathogens being destroyed by the immune system before the host cells are infected and viral replication has begun and is the basis for long-lasting immunity.
COVID-19 Vaccines
A mRNA vaccine is the most common vaccine type for COVID-19. A mRNA vaccine involves a lipid nanoparticle (similar to a biological membrane) that allows the vaccine genetic material to enter human cells. This mRNA codes for the SARS-CoV-2 spike protein. Our cells translate the mRNA into spike proteins.
These spike proteins then interact with B-cells, which in turn produce antibodies that are specialized to attach to the SARS-Cov-2 spike protein. Since memory B-cells will trigger a rapid adaptive immune response when a SARS-CoV-2 virus is detected, the host is more likely to experience less severe symptoms than if they had not been vaccinated.
Treatments
Monoclonal antibodies have been effective in treating patients with life threatening COVID-19 infections. These are the same as the antibodies that can be created by B-cells. When injected into a patient, these antibodies attach to SARS-CoV-2 spike proteins, not allowing the virus to infect host cells and identifying the virus as a threat to other white blood cells. Similar treatments are also used to combat autoimmune diseases and some forms of cancer.