SARS-CoV-2 (gold) emerging from cells (green/purple).
How did Covid-19 become a global pandemic, and how can researchers develop vaccines that would give people immunity to the SARS-CoV-2 coronavirus?
Answering both questions requires understanding how the human body responds to infection by SARS-CoV-2 — and science suggests that the secrets to the virus' success lies in its ability to suppress certain parts of your immune system.
Defences against disease-causing germs — pathogens — consist of two systems: innate and adaptive. The innate immune system responds to general threats after detecting molecular patterns characteristic of microbes, such as certain sugars on bacteria, while the adaptive immune system learns to recognize and remember specific pathogens. Together they create immunity — protection from infection.
Innate immune responses
Your body's first lines of defence against invading pathogens such as viruses is the innate immune system, which includes skin and other barriers, molecules like antiviral 'interferons', and white blood cells.
The innate system responds by immediately, deploying its weapons to the site of infection, which can cause inflammation. Some white blood cells act as sentinels to watch out for invaders and certain types — such as macrophages and dendritic cells — will eat and digest pathogens through phagocytosis.
Research suggests that the innate immune response to SARS-CoV-2 is similar to that for its cousins, fellow coronaviruses SARS-CoV-1 and MERS-CoV (which cause Severe Acute Respiratory Syndrome and Middle East Respiratory Syndrome).
Like its relatives, SARS-CoV-2 suppresses the immune system by disrupting the actions of immune cells and interferon molecules. That immunosuppression ability might explain why Covid-19 has such a long incubation period — up to two weeks — compared to influenza (1-4 days).
Immunosuppression probably explains why Coronavirus is able to wreck havoc on the innate system, recruiting too many white blood cells and causing excessive inflammation. That inflammatory response might then in turn lead to the 'acute respiratory distress syndrome' that causes shortness of breath and lung injury in severe cases of coronavirus disease.
Adaptive immune responses
Your body's second source of protection is the adaptive immune system, which includes B cells that release antibodies and T cells that kill to new invaders and remember old enemies.
Compared to the innate response, the adaptive system responds slowly. It builds-up immunity over a few days, not hours, but then kills or neutralizes a pathogen that tries to reinfect you. The system develops an immunological memory of the invader so that, in future, it's able to quickly fight-off repeated invasions.
Antibodies and B cells
Antibodies that match and bind to antigen molecules are produced by B cells. Anything covered with a specific antigen — such as a virus particle with that antigen on its surface — is effectively tagged as 'enemy'.
Once attached to matching antigens, antibodies might physically block a microbe from invading your cells (neutralisation), allow the invader to be more easily ingested by phagocytes (opsonisation) or mark it for destruction by a team of enzymes (called 'complement') or executioners such as Natural Killer cells.
Covid-19 tests can detect antibodies against SARS-CoV-2 within 1-2 weeks after an infected person develops symptoms. Those antibodies usually match the spike protein that a coronavirus uses to break into your cells.
How long does immunity last? While we don't yet know for the SARS-CoV-2 virus, studies of SARS patients have detected antibodies against SARS-CoV-1 over two years following infection.
Antigens and T cells
Following invasion by a pathogen, dendritic cells ingest that germ's antigens and travel to lymph nodes, where they do their job as a 'professional antigen-presenting cell' (APC) and show the foreign antigens to T cells. Once activated, the T cells divide and circulate in your bloodstream, ready to recognize and fight any invaders they might encounter.
SARS-CoV-2 infection and the development of immunity.
Like other parts of the adaptive immune system, T cells can recognize a foreign antigen — but only when it's presented on the surface of an infected cell. They come in two types: 'cytotoxic T lymphocytes' (CTL) that kill microbes or virus-infected body cells using destructive molecules, and 'helper T cells' (Th) that aid other immune cells — helping B cells generates antibodies, for example.
Those interactions between the various cells can be seen in the above figure from a recent review in The Lancet.
After T cells help eliminate a pathogen, some remain in your body as long-lived 'memory T cells' that can be reactivated to rapidly respond if the same pathogen invades again. Activating T cells therefore results in much stronger immunity.
Although current vaccines against influenza and measles viruses are effective despite the fact that they only prompt the immune system to generate antibodies, evidence suggests that immunity against SARS-CoV-2 also requires T cells.
A study of 20 patients who recovered from Covid-19 found that they all carried helper T cells that recognize the SARS-CoV-2 spike-protein antigen, and 70% had cytotoxic T cells (the type that kills infected cells) matching the virus.
As with SARS and MERS, studies have found that SARS-CoV-2 can delay the activation of T cells, especially the cytotoxic type — another example of the virus' ability to evade immune responses, which might contribute to Covid-19's long incubation time. During that presymptomatic period, you could still be infectious — shedding virus particles and transmitting the disease.
Add the number of presymptomatic cases to people who might never show symptoms — asymptomatic carriers — and you end-up with a major contributing factor that explains how Coronavirus managed to spread across the world.
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2020-11-30 00:25:15Z
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