As the notorious coronavirus continues to wreak havoc, it might make you wonder how it manages to use subterfuge and evades our immune system.
To understand the basic trajectory of the virus we must first know how our immune system works.
Defences against any disease - caused by harmful pathogens – consist of two system: Innate and Adaptive Immune Response.
The innate immune system responds to general threats after detecting molecular patterns like microbes, while the adaptive immune system learns to recognize and remember specific pathogens. And together they create immunity — protection from infection.
Body's first line of defence is the innate immune system, which includes skin and other barriers, 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. The white blood cells act as sentinels to watch out for invaders — such as macrophages and dendritic cells — to digest them through phagocytosis.
Like other coronaviruses, SARS-CoV-1 and MERS-CoV (which cause Severe Acute Respiratory Syndrome and Middle East Respiratory Syndrome), covid-19 or SARS-CoV-2 can suppress the immune system by disrupting the actions of immune cells and interferon molecules.
In the case of Covid-19 the immunosuppression ability has been high making its incubation period longer - up to two weeks — compared to influenza (1-4 days).
This longer incubation period or immunosuppression ability is the reason for recruiting too many white blood cells and therefore 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.
The second source of body protection - Adaptive immune system - includes B cells that release antibodies and T cells that kill new invaders and remember old enemies.
Compared to the innate response, the adaptive system responds slowly. It builds-up immunity over a few days and 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.
First, the B cell produces antibodies that identify any particle as 'enemy' if covered with a specific antigen on its surface. It then match and bind to antigen molecules to block a microbe from invading cells by neutralization, 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.
Within 1-2 week after an infected person develops symptoms, antibodies against SARS-CoV-2 can be detected through Covid-19 tests. Those antibodies usually match the spike protein that a coronavirus uses to break into your cells.
Although it is yet to be known how long does the immunity last for SARS-CoV-2 virus but previous studies of SARS patients have detected antibodies against SARS-CoV-1 that lasted over two years following infection.
Following invasion by a pathogen, the germ's antigens do their job as a 'professional antigen-presenting cell' (APC) and show the foreign antigens to T cells. They can recognize a foreign antigen only when it's presented on the surface of an infected cell.
Once activated, the T cells divide and circulate in your bloodstream, ready to recognize and fight any invaders they might encounter.
T cells 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 —like helping B cells generate antibodies.
After T cells help eliminate a pathogen, some remain in the 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.
Study suggests that immunity against SARS-CoV-2 also requires T cells, while current vaccines against influenza and measles viruses are effective despite the fact that they only prompt the immune system to generate antibodies.
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 that killed infected cells matching the virus.
Moreover, the studies have found that SARS-CoV-2 can delay the activation of T cells, especially the cytotoxic type — another strategy of the virus to evade immune responses - which might contribute to Covid-19's long incubation period.
During that presymptomatic period, one could still be infectious — shedding virus particles and transmitting the disease. And when the number adds to the asymptomatic carriers, it explains how covid-19 managed to turn into the deadliest pandemic in history.