Last updated on April 24, 2020
We’ve talked a lot about Covid-19 the past couple weeks — what type of virus it is and how it spreads. What I haven’t touched on yet is what viruses actually are and how they work. Virus is a broad category referring to genetic material (DNA or RNA) encased in a protein shell. Viruses don’t contain any cellular machinery of their own and therefore cannot replicate themselves nor their genetic material. Instead, they inject their genetic material into a cell and hijack the cell’s machinery to construct copies of the virus.
This process can end with complete cell lysis (breaking open and deflating like a water balloon with holes), which allows the new virus particles to leave the cell and infect new hosts. Or the process can end with the new virus budding out of the cell, covered in a layer of cellular membrane. In some cases, the viral genetic material incorporates itself into the host’s DNA, where it lies dormant and replicates as the host cell replicates. Eventually, the viral genetic material is activated, viral proteins are constructed, and the virus leaves the cell either through lysis or budding.
Viruses are extraordinarily adaptable. Studies have shown that, when faced with an obstacle to reproduction, viruses can evolve to overcome that obstacle in just two weeks. Because viruses replicate so quickly and voluminously in a host, random mutations (small changes in genetic material due to errors in replication) and recombination (larger changes in genetic material due to genetic exchange between two different viruses) are extremely common. These changes in the viral genetic material undergo strong selective pressure (survival-of-the-fittest) so that mutated viruses that cannot efficiently infect cells, replicate, and propagate die out quickly.
The combination of random genetic change and selective pressure is what makes it possible for viruses to jump from infecting one species to another. This process, called zoonotic spillover, requires many specific variables to be successful. Most mutated viruses that attempt to jump species don’t have the right efficiency, transmissibility, or severity to make the jump and become an epidemic.
The speed of viral evolution means that viruses are already incomparably diverse. It is impossible to know just how many different virus species there actually are (for one thing, you would have to define what “different” means in this context). The vast majority of viruses are bacteriophages, viruses that only attack bacterial cells. Bacteriophages are usually equipped to attack a specific type of bacteria. Bacteria are in a never ending evolutionarily race with bacteriophages; bacteria are constantly evolving new lines of defense, like the one that facilitates CRISPR-Cas9 (but more on that later), and bacteriophages are always evolving new forms of attack. This arms race may yet be the key to treating obstinate bacterial infections in humans. The capability of bacteria to evolve overtime and the abuse of antibiotics has led to a rise in antibiotic resistance, but studies indicate that bacteriophages could be used for targeted therapy of antibiotic resistant infections. For more information about bacteriophages, check out this video by “Kurzgesagt – In a Nutshell”:
Viruses are often categorized by what type of genetic material they contain in a system called the Baltimore classification. Class I refers to viruses with double-stranded DNA including adenoviruses, herpesviruses, and poxviruses, which can cause acute respiratory illnesses, herpes/chickenpox, and smallpox respectively. Class I viruses can only replicate themselves in cells that are currently replicating because replication of double-stranded DNA requires enzymes that the cell only produces during its own replication.
Class II refers to viruses with single-stranded DNA including parvoviruses, a virus family that is mainly known to infect dogs, but that can also infect humans causing mild rashes.
Class III refers to viruses with double-stranded RNA including rotavirus, which can cause severe gastrointestinal symptoms.
Class IV refers to viruses with “positive sense” (the strand that can be directly translated into protein) single-stranded RNA including coronaviruses (that old chestnut), picornaviruses, and togaviruses. Coronaviruses, as we know, can cause SARS, MERS, or cold-like symptoms. Picornaviruses are responsible for a wide range of human diseases including meningitis, polio, hepatitis A, and the common cold. Togaviruses mainly cause rubella in humans.
Class V refers to viruses with “negative sense” (the strand that must be transcribed into positive sense before proteins can be constructed) single-stranded RNA including orthomyxoviruses and rhabdoviruses, which cause the flu and rabies respectively.
Class VI refers to viruses with “positive sense” single-stranded RNA that must be turned into DNA via an enzyme called reverse transcriptase before the virus can be replicated. Class VI includes retroviruses, the most famous of which is HIV. Retroviruses use reverse transcriptase to turn its RNA into DNA that is integrated into the host cell’s DNA. From there, it can use the cell’s machinery to make copies of its genetic material and create proteins for a new virus.
Class VII refers to viruses with double-stranded DNA that forms a closed circle. In order to replicate, this closed circle is transcribed into RNA, which must then be converted back into DNA using the reverse transcriptase enzyme. Class VII includes Hepadnaviruses, which can cause Hepititis B.
Hope you enjoyed that little dive into the world of viruses! Comment below or email me at contact@anyonecanscience.com to let me know what you think about this week’s blog post and tell me what sorts of topics you want me to cover in the future. And subscribe below for weekly science posts sent straight to your email!
