Viruses are puzzling. These tiny parasites aren’t really alive, but they aren’t inactive either. They’ve flourished and mutated throughout the years, achieving astounding rates of diversity yet are surprisingly simple in structure. Despite being the main perpetrator of some of the world’s largest pandemics, such as COVID-19, there is still much that is unknown about a virus’s transmission and method of infection.
While viruses have sophisticated infiltration systems and detrimental health effects, the structure of a virus is relatively simple. Every virus consists of two parts: Nucleic acid, which holds genetic information, and a surrounding protein shell called a capsid. Capsids are extremely small and can be about 10,000 times smaller than a grain of salt.
Some, such as the SARS-CoV2 virus which causes the COVID-19 infection, are also enclosed by an additional lipid envelope. However, this envelope membrane melts away in the presence of soap, causing a lipid-to-lipid interaction and forcing parts of the membrane to break apart, which essentially “kills” the virus. To viruses like these, this second envelope leads to both vulnerability and additional means of transmission.
“Higher temperatures and lower humidity are going to allow less time for the [enveloped] virus to be in a transmissible form in the environment,” said Prof. Hector Aguilar-Carreno, microbiology and immunology, who works on antivirals and vaccines, focusing on cellular factors involved in viral replication.
Because viruses have such a simple structure, they cannot reproduce, and are therefore not considered “living.” Instead, it finds a host to carry out its replication and spreads its copies throughout the body.
To identify an appropriate host cell, viruses have proteins on their surfaces that correspond to receptors on their target cell. Once connected, the virus can transmit its genetic material into the host cell, and hijack the cell’s molecular machinery to read and build more copies of the virus.
Inside the host body, newly formed viruses repeat this process, infiltrating surrounding cells and recruiting them to create more copies of the virus. These massive replication cycles create armies of viruses that can cause symptoms as mild as a cough or as fatal as organ failure.
In the case of the COVID-19 disease, symptoms include coughing, shortness of breath and other respiratory problems which can lead to lung failure. Like other viruses, the SARS-CoV2 virus can cause disease directly and indirectly through destroying cells in the lung when they replicate, according to Prof. Cedric Feschotte, molecular biology and genetics. Feschotte studies endogenous viruses — viral DNA in the human genome — and transposons — a jumping gene that can facilitate viral infections across many species.
“But oftentimes that’s not what really causes the most problems. The problems, paradoxically, are caused by the response, the immune response to the virus, the first line of response which is inflammation,” Feschotte said. “It’s a mix of infection and inflammation together that’s really bad.”
According to Aguilar-Carreno, how a virus spreads from human to human depends on the type of virus. Many, such as the influenza virus, can travel through respiratory droplets that fly from a person’s mouth every time they cough. They can survive longer in cool, dry environments, which is why flu season is in the winter.
Viruses cannot survive at high temperatures, and a fever is believed to be a way for the body to kill the virus. Other viruses spread through bodily fluids, like HIV.
Though some viruses can infect one species, many viruses responsible for large scale outbreaks have transferred from animals to humans, known as zoonotic diseases. There is evidence that the SARS outbreak in 2002 and similar coronavirus strains like it spread from horseshoe bats. In order for a virus to jump from a bat to a human, the receptors in the bat cells must be closely related to the receptors in humans, In the case of the coronavirus, the protein on the virus binds to the cell receptor, leading to entry into a lung cell.
In addition to targeting multiple species, viruses can attack multiple organs within species, if there are receptors and other necessary proteins for that virus at different locations in the body. Viruses can use the bloodstream to travel to different parts of the body to infect these areas. Mutations in viruses can also lead to a broader range of target species, and as humans become infected by viruses, our cells are slowly changing to escape them.
“There is a coevolution. Oftentimes, [cell] receptors are trying to escape being recognized by viruses and the virus is trying to catch up and reorganize. It leads to this kind of arms race or evolution battle,” Feschotte said.
Despite our body’s ability to evolve, the rate of evolution in viruses is faster. For example, the flu mutates at a rapid rate, requiring a new vaccine every year to prevent infection. As for the novel coronavirus, mutations do not seem to happen as fast, which is good news for those who are developing treatments.
Yet it is still possible for the SARS-CoV2 virus to mutate before a vaccine rolls out.
“Yes,” Aguilar-Carreno said. “With viruses, anything is possible.”