Contents
The first electronic photographs and illustrations created from them, which show the structure of the coronavirus that caused the COVID-19 pandemic, appeared in February 20201. Since then, scientists have studied the enemy in sufficient detail, although he continues to mutate and much about him still remains unknown. Let’s discuss in more detail what scientists know about the inner workings of the pathogen that hit the world today.
Despite all the remaining mysteries surrounding the novel coronavirus and the disease it causes, COVID-19, scientists have amassed an incredible amount of detailed knowledge in a surprisingly short time.
Thousands of different coronaviruses can live on the planet. Four of them are the cause of respiratory diseases that occur like banal colds. Two others have already caused alarming outbreaks: in 2002, the coronavirus caused severe acute respiratory syndrome (SARS), which killed more than 770 people worldwide, and in 2012, another strain caused Middle East respiratory syndrome (MERS), which killed more than 800 people. . SARS virtually disappeared within a year; MERS still persists2.
The newest coronavirus, SARS-CoV-2, has caused a much deadlier pandemic in part because it can go unnoticed for a long time after it infects a person (asymptomatic and long incubation period, and long virus isolation period). A person who had the SARS coronavirus transmitted it within 24 to 36 hours of developing symptoms such as fever and dry cough; and people who don’t feel well can be isolated before they infect others.
But people with COVID-19 can transmit the virus before they have obvious symptoms. Without feeling sick, infected men and women work, drive, shop, eat out, and attend parties while exhaling the coronavirus into the airspace of those around them. The virus can go undetected inside the human body for so long, in part because its genome produces proteins that keep our immune systems from sounding the alarm. Meanwhile, lung cells are dying as the virus secretly replicates and damages them. When the immune system recognizes viral particles, it can go into cytokine storm mode, further damaging the cells it is trying to save.
Coronaviruses are relatively simple viral structures, and their shape and appearance help us understand how they work. They are spherical and covered in spikes with a spike protein. These spikes help the virus bind to healthy cells and infect them.
However, the same spines (protrusions containing proteins) also allow the immune system to “see” the virus. Parts of the spike protein could be used in potential coronavirus vaccines to induce the body to produce antibodies against this new virus.
In fact, coronaviruses are named after the distinctive appearance of their spines; under a powerful microscope, the spikes look like a crown (hence the name coronavirus). Beneath these spikes is a layer of membrane. This membrane can be damaged by disinfectants, detergents, and alcohols, so soap, water, and alcohol-based hand sanitizer gels are effective against the virus.
Inside the membrane is the genetic material of the virus – its genome. According to the composition of the genome, all viruses are divided into two groups – DNA-containing, such as the chickenpox virus, and RNA viruses (these include coronavirus). RNA viruses have small genomes that are subject to constant change. These changes, called mutations, help the virus adapt to and infect new host species. It is believed that the new COVID-19 probably originated from a bat virus, but it is not yet known whether the mutations allowed this transition from animals to humans (or were there other interventions).
The SARS-CoV-2 genome is a strand of RNA that is about 29 bases long, almost the limit for RNA viruses. The flu has about 900 bases, and the rhinoviruses that cause the common cold have about 13 bases. (A base is a pair of nucleotide compounds that are the building blocks of RNA and DNA.) Because the genome is so large, many mutations can occur during replication (copy making) that will harm the virus, but SARS-CoV-500 can compute and fix copies . Such quality control is common for human cells and DNA viruses, but very unusual for RNA viruses. The long genome also has accessory genes that are not fully understood, but some of which may help it counter our immune system.3.
The novel SARS-CoV-2 is most closely related to the SARS-CoV group of viruses found in humans, bats, lizards and civets. Despite this, there are also differences between the new COVID-19 and the virus that caused the SARS epidemic (in the past epidemic) due to changes in their genomes. This includes how they are passed from one person to another and the various symptoms of the disease. Initially, the new coronavirus was thought to be more contagious than the virus that caused SARS, but less likely to cause serious illness. However, the emergence of more and more aggressive mutations (British, Indian, and now Brazilian strains) refutes this assertion.
How does the immune system react to the virus?
Because this virus is new, no one is immune to it. This means that it will potentially infect a very large number of people (virtually until all people in one way or another do not get sick or acquire post-vaccination immunity, we will get sick). Yes, the number of very severe cases is small in percentage terms (although new strains behave more aggressively), but people suffer from the disease with a lot of unpleasant manifestations and complications, it is extremely difficult to predict the course of the disease.
When SARS-CoV-2 infects a person, it enters the nose or mouth, and circulates, multiplies in the respiratory tract, until it touches the lung cell, on the surface of which the ACE2 receptor is located. The virus binds to that cell, slips in and uses the cell’s internal mechanisms to make copies of itself. When enough viral particles accumulate, they break out, leaving the cell to die, and enter other cells. Infected cells send signals to the immune system to try to neutralize or destroy pathogens, but viruses can prevent or intercept the signals, buying them time to replicate widely before the first symptoms appear.4.
Virus drugs and vaccines
More than 100 drugs are being researched by commercial and university laboratories around the world to fight COVID-19, the disease caused by the SARS-CoV-2 virus. Most drugs do not directly kill the virus, but interfere with it enough to allow the body’s immune system to clear the infection. Antivirals usually prevent a virus from attaching to a lung cell, prevent a virus from multiplying if it does invade a cell, or dampen an overreaction of the immune system that can cause severe symptoms in infected people (cytokine storm)5.
Vaccines prepare the immune system to quickly and effectively fight a future infection by simulating an infectious process without the presence of a live virus in the body.
How COVID-19 Spreads
The main route of transmission of the new coronavirus is through the air, through small droplets emitted when coughing, sneezing or talking, as well as through aerosols (smaller droplets that can travel further and remain suspended in the air) that accumulate in closed and poorly ventilated areas. The virus can also be transmitted by touching the eyes, nose, or mouth after touching contaminated surfaces, although this route of transmission appears to be rare.
Unlike SARS, which is only transmitted from people with symptoms, the new coronavirus can be transmitted a day or two before symptoms appear (presymptomatic) or even from people who never develop clinical symptoms (asymptomatic). This greatly hinders efforts to contain the spread of viruses, and is the reason why everyone should wear a mask and practice social distancing.
These viruses can be easily transmitted from one person to another. To date, the WHO estimates that R0, or the basic reproduction number of the virus, is somewhere between 1,4 and 2,5, although other estimates give a range of 2 to 3. This means that each infected person can, in their own turn, infect 2-3 other people, although there are “superspreaders” infecting more people. To control an epidemic, R0 must be below 1.
How COVID-19 is diagnosed
To identify active infections, you need to look for the virus itself: SARS-Cov2 infection occurs mainly in the respiratory tract. This is why diagnostic tests based on the amplification of viral gene sequences by PCR should be performed on swabs from the nose or throat. It is important to remember that PCR tests do not distinguish between viable virus and viral fragments. In addition, the result may depend on how the sample is taken. Other diagnostic tests detect viral proteins (rapid antigen tests) – they are less sensitive (i.e. they do not detect everyone who is infected), but faster and easier to use, and can identify people with a high viral load and therefore highly contagious.
To prove past infections, look for antibodies. Another type of test detects virus-specific antibodies. In this case, a blood sample is sufficient. This test identifies people who have been previously exposed to the virus and may therefore be immune. Serological tests currently in use vary widely in terms of sensitivity (ability to detect positive cases) and specificity (ability to distinguish from other viruses), so the results should be interpreted with caution. In addition, the presence of antibodies to the virus does not guarantee immunity to it. Conversely, cellular immunity (virus-specific T cells) is observed even in recovered patients with undetectable antibodies.
Sources:
- Cui J, Li F, Shi ZL. Origin and evolution of pathogenic coronaviruses. Nature Reviews Microbiology. 2019 Mar;17(3):181-192. DOI: 10.1038/s41579-018-0118-9.
- Wu F, Zhao S, Yu B, et al. A new coronavirus associated with human respiratory disease in China. Nature. 2020 Mar;579(7798):265-269. DOI: 10.1038/s41586-020-2008-3.
- Zhou P, Yang XL, Wang XG, et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature. 2020 Mar;579(7798):270-273. DOI: 10.1038/s41586-020-2012-7.
- Andersen KG, Rambaut A, Lipkin WI, Holmes EC, Garry RF. The proximal origin of SARS-CoV-2. Nature Medicine. 2020 Apr;26(4):450-452. DOI: 10.1038/s41591-020-0820-9.
- Corman VM, Muth D, Niemeyer D, Drosten C. Hosts and Sources of Endemic Human Coronaviruses. Advances in Virus Research. 2018;100:163-188. DOI: 10.1016/bs.aivir.2018.01.001.