On Sept. 16, 2020, a study by researchers at La Jolla Institute for Immunology published in the Cell, confirmed that a multi-layered, virus-specific immune response is important for controlling the virus during the acute phase of the infection and reducing COVID-19 disease severity, with the bulk of the evidence pointing to a much bigger role for T cells than antibodies.

A weak or uncoordinated immune response, on the other hand, predicted a poor disease outcome. The findings suggest that vaccine candidates should aim to elicit a broad immune response that include antibodies, helper and killer T cells to ensure protective immunity.

When SARS-CoV-2 (or any other virus) infiltrates the body, the innate immune system is first on the scene and launches a broad and unspecific attack against the intruder. It releases waves of signaling molecules that incite inflammation and alert the immune system’s precision forces to the presence of a pathogen.

Within days, the so-called adaptive immune system tools up and moves with pinpoint precision against the virus, intercepting viral particles and killing infected cells.

The adaptive immune system consists of three branches: antibodies; helper T cells (Th), which assist B cell to make protective antibodies; and killer T cells (CTL), which seek out virus-infected cells and eliminate them.

For their latest study, the researchers collected blood samples from 50 COVID-19 patients and analyzed all three branches of the adaptive immune system—SARS-CoV-2 specific antibodies, helper and killer T cells—in great detail.

If a vaccination is successful, vaccine-induced antibodies are ready to intercept the virus when it shows up at the doorstep. In contrast, in a normal infection the virus gets a head start because the immune system has never seen anything like it. By the time the adaptive immune system is ready to go during a primary infection, the virus has already replicated inside cells and antibodies can’t get to it.