{"id":120,"date":"2020-04-10T12:00:00","date_gmt":"2020-04-10T16:00:00","guid":{"rendered":"http:\/\/anyonecanscience.com\/?p=120"},"modified":"2020-04-24T11:59:25","modified_gmt":"2020-04-24T15:59:25","slug":"the-wonderful-world-of-viruses","status":"publish","type":"post","link":"https:\/\/anyonecanscience.com\/index.php\/2020\/04\/10\/the-wonderful-world-of-viruses\/","title":{"rendered":"The Wonderful World of Viruses"},"content":{"rendered":"\n

         We\u2019ve talked a lot about Covid-19 the past couple weeks \u2014 what type of virus it is and how it spreads.  What I haven\u2019t 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\u2019t 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\u2019s machinery to construct copies of the virus. <\/p>\n\n\n\n

         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\u2019s 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.  <\/p>\n\n\n\n

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Visualization of cell lysis following viral replication<\/figcaption><\/figure>\n\n\n\n

         Viruses are extraordinarily adaptable. Studies have shown<\/a> 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<\/a>. 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.   <\/p>\n\n\n\n

         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<\/a>, 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.<\/p>\n\n\n\n

         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 \u201cdifferent\u201d means in this context). The vast majority of viruses are bacteriophages<\/a>, 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<\/a> of antibiotic resistant infections. For more information about bacteriophages, check out this video by \u201cKurzgesagt \u2013 In a Nutshell\u201d:<\/p>\n\n\n\n

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