How Viruses Work

Anatomy of a Virus

Viruses travel light.

They have a core of genetic information

surrounded by a protein shell.

Some have an oily outer layer called an envelope.

These parts form an efficient delivery system. And when it comes down to it, that’s all a virus is—a package of genetic cargo that needs to be delivered to a host cell so the virus gets copied.

A virus’s genetic information holds its genes.

Each gene is a set of instructions for making a viral protein.

In fact, a virus has a gene for every protein needed to make more virus.

An Infection Begins

Viruses can’t reproduce, or copy themselves, on their own. They need one more thing—you!

It’s your cells that make copies of the virus, which is why you get sick. Here’s an up-close look at how an infection starts.

Like all cells, this airway cell has a membrane. It’s an oily layer that surrounds the cell and keeps bad things out.

But proteins on the surface of the virus help it get through the membrane.

The viral surface proteins “lock on” to receptor proteins on the airway cell.

If the fit between the virus and host cell is a match, the virus slips into the host cell.

The Virus Spreads

Once inside a host cell, the virus releases its genetic information.

Then the host cell goes to work! But instead of doing its regular job, it uses its machinery and resources to make new viruses.

The host cell makes many copies of the virus’s genetic information.

Then, it reads the copies to make huge amounts of viral proteins.

The new parts are packed into new viruses and released from the cell.

The infection spreads to nearby cells. Each newly infected cell becomes another virus-building factory.

Viral Proteins Only Unlock Specific Cells

A virus can’t spread to just any cell. Each type of virus has surface proteins that fit only with certain parts (called receptors) on the host cell surface.

And not all cells are the same. Your body is made up of thousands of different cell types, each with its own mix of receptors.

A virus can enter a cell only if the right receptors are there.

Inside Interactions

Getting into a cell is just the first step of an infection. Once inside, the virus must interact with even more host cell parts to be able to reproduce.

Take SARS-CoV-2 coronavirus, for example. To get into cells, it uses a receptor that’s found all over your body. But it can’t reproduce in all these places.

To reproduce, the virus needs to also fit with parts inside the host cell. The process involves hundreds of host cell proteins! And only some cell types have all the right parts to fit with SARS-CoV-2. If the virus and cell aren’t a fit at every step, it’s a dead end for the virus. If it can’t reproduce, it can’t spread.

Different Cells, Different Symptoms

You probably know that no two viruses make you sick the same way. It goes back to which cell types they infect.

For example, rhinovirus (one cause of the common cold) infects airway cells. So you sneeze and have a runny nose. Norovirus (a cause of food poisoning or the “stomach flu”) infects cells in your gut. So you get an upset stomach, nausea, and diarrhea.

Many symptoms arise because copying the virus harms your cells. A cell’s resources get used up as it pumps out tons of new viruses, so it can’t do its regular job very well. Most viruses eventually kill their host cells, causing you pain and swelling in the area.

With some viruses, you feel symptoms in places outside of where the virus infects. For example, influenza A only infects your airways. But if you’ve ever had the flu, you know it makes you feel bad all over. People often have airway symptoms combined with headaches, fever, sore muscles, and low energy.

These symptoms are side effects from your immune system as it kills the virus. That’s why the symptoms happen with many illnesses.

Every Copy is a Chance to Change

Viruses multiply quickly. A single infected cell can make thousands of new viruses. And each of those can spread to new cells. Within days, an infected person can make millions or even billions of viruses.

Each time a virus’s genetic information is copied, there’s a chance an error called a mutation can happen. Some mutations change viral proteins and affect what the virus can do—like what species it can infect or how well it resists host defenses.

To learn more, visit How Viruses Evolve.

Viruses Only Infect Compatible Host Species

Viruses aren’t only specific when it comes to the host cells they infect. They infect specific host species too. While some viruses only infect one species, others infect multiple species.

Again, it all comes down to a good fit between the virus and the parts of the host cell. For example, some viruses interact with surface proteins found in just one species. Others interact with surface proteins that are very similar across multiple species. Just like with cell type specificity, the virus and host cell parts must fit through every step of the infection cycle.

But, whether they infect one or multiple host species, the result is the same. The virus takes over cells within their host. Then they use the cell’s machinery, energy, and resources to make more viruses and spread.

Some viruses do gain the ability to infect new species. To learn more, visit When Viruses Jump Hosts.

The virus on the left fits with a surface receptor that’s only on human cells; it can’t infect pigs or ducks. The one on the right fits with a surface receptor that’s very similar in humans, pigs, and ducks—so it can infect all three.

References

Baraniuk, C. (2020). Receptors for SARS-CoV-2 present in wide variety of human cells. The Scientist Magazine.

Elizabeth, R., Stan, D., & Pinsky Benjamin, A. (2015). Norovirus. Clinical Microbiology Reviews, 28(1), 134-64.

Jacobs, S. E., Lamson, D. M., George, K. S., & Walsh, T. J. (2013). Human rhinoviruses. Clinical microbiology reviews, 26(1), 135-162.

Muus, C., Luecken, M. D., Eraslan, G., Waghray, A., Heimberg, G., Sikkema, L., ... & Jagadeesh, K. (2020). Integrated analyses of single-cell atlases reveal age, gender, and smoking status associations with cell type-specific expression of mediators of SARS-CoV-2 viral entry and highlights inflammatory programs in putative target cells. BioRxiv.

The hunt for COVID-19 treatments has researchers optimistic. (2020, August 20). American Heart Association News. https://www.heart.org/en/news/2020/08/20/the-hunt-for-covid-19-treatments-has-researchers-optimistic

Walls, A. C., Park, Y. J., Tortorici, M. A., Wall, A., McGuire, A. T., & Veesler, D. (2020). Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein. Cell. 181(2):281-292.

Warren, C. J., Meyerson, N. R., Dirasantha, O., Feldman, E. R., Wilkerson, G. K., & Sawyer, S. L. (2019). Selective use of primate CD4 receptors by HIV-1. PLoS biology, 17(6), e3000304.

Zhang, Y., Geng, X., Tan, Y., Li, Q., Xu, C., Xu, J., Hao, L., Zeng, Z., Luo, X., Liu, F., & Wang, H. (2020). New understanding of the damage of SARS-CoV-2 infection outside the respiratory system. Biomedicine & pharmacotherapy 127, 110195.