Inside the Coronavirus
What scientists know about the inner workings of the pathogen that has infected the world
For all the mysteries that remain about the novel coronavirus and the COVID-19 disease it causes, scientists have generated an incredible amount of fine-grained knowledge in a surprisingly short time.
In the graphics that follow, Scientific American presents detailed explanations, current as of mid-June, into how SARS-CoV-2 sneaks inside human cells, makes copies of itself and bursts out to infiltrate many more cells, widening infection. We show how the immune system would normally attempt to neutralize virus particles and how CoV-2 can block that effort. We explain some of the virus's surprising abilities, such as its capacity to proofread new virus copies as they are being made to prevent mutations that could destroy them. And we show how drugs and vaccines might still be able to overcome the intruders. As virologists learn more, we will update these graphics on our Web site (www.scientificamerican.com).
For a static version of this content as it appears in the July 2020 issue of Scientific American, please click here.
A SARS-CoV-2 virus particle wafting into a person's nose or mouth is about 100 nanometers in diameter--visible only with an electron microscope. It is a near sphere of protein (cross section shown) inside a fatty membrane that protects a twisting strand of RNA--a molecule that holds the virus's genetic code. Proteins called "S" form spikes that extend from the surface and grab onto a human cell, hundreds of times larger, so the particle, or virion, can slip inside; the crown, or corona, appearance gives the virus its name. Structural proteins--N, M and E--move inside the cell, where they help new virions form.
- 1. The virus: The SARS-CoV-2 virus particle is a ball of proteins wrapped in a protective fatty coating.
- 2. RNA (red): This twisting strand of RNA is the blueprint the virus uses to replicate itself inside of you.
- 3. Entry spikes (Orange): The virus uses its spike-shaped S proteins, which stud the surface, to grab onto human cells.
- 4. Protective shell: This lipid bilayer protects the virus's genetic cargo as it travels inside the body.
- 5. N Protein (Blue): This protein helps keep the viral RNA stable.
- 6. E Protein (Yellow): This protein helps new virus particles form.
- 7. M Protein (Purple): This protein helps new virus particles form.
A SARS-CoV-2 particle enters a person's nose or mouth and floats in the airway until it brushes against a lung cell that has an ACE2 receptor on the surface. The virus binds to that cell, slips inside and uses the cell's machinery to help make copies of itself. They break out, leaving the cell for dead, and penetrate other cells.
Additional vesicles (that come from the endoplasmic reticulum and Golgi complex) assemble spike, M and E proteins.
Infected cells send out alarms to the immune system to try to neutralize or destroy the pathogens, but the viruses can prevent or intercept the signals, buying time to replicate widely before a person shows symptoms. When infection begins, the innate immune system tries to immediately protect lung cells. The adaptive immune system gears up for a greater response.
Tactic 1: The virus spike may camouflage itself with sugar molecules. They flex and swing, potentially blocking antibodies from attaching to the virus, neutralizing it.
Commercial and university labs are investigating well over 100 drugs to fight COVID-19, the disease the SARS-CoV-2 virus causes. Most drugs would not destroy the virus directly but would interfere with it enough to allow the body's immune system to clear the infection. Antiviral drugs generally stop a virus from attaching to a lung cell, prevent a virus from reproducing if it does invade a cell, or dampen an overreaction by the immune system, which can cause severe symptoms in infected people. Vaccines prepare the immune system to quickly and effectively fight a future infection.
The SARS-CoV-2 genome is a strand of RNA that is about 29,900 bases long--near the limit for RNA viruses. Influenza has about 13,500 bases, and the rhinoviruses that cause common colds have about 8,000. (A base is a pair of compounds that are the building blocks of RNA and DNA.) Because the genome is so large, many mutations could occur during replication that would cripple the virus, but SARS-CoV-2 can proofread and correct copies. This quality control is common in human cells and in DNA viruses but highly unusual in RNA viruses. The long genome also has accessory genes, not fully understood, some of which may help it fend off our immune system.
- Editor: Mark Fischetti
- Artist: Veronica Falconieri Hays
- Consultant: Britt Glaunsinger, molecular virologist, University of California, Berkeley, and Howard Hughes Medical Institute
- Graphics Editor: Jen Christiansen
- Animation and Motion Graphics: Jeffery DelViscio
- Design and Front-end Development: Jason Mischka
- Sources: Lorenzo Casalino, Zied Gaieb and Rommie Amaro, U.C. San Diego (spike model with glycosylations);
- "The Architecture of SARS-CoV-2 Transcriptome," by Dongwan Kim et al., in Cell, Vol 181, May 14, 2020 (genome)
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