One base will pair and bind with the other base. But sometimes mutations occur if a wrong pairing happens. If A by mistake ends up pairing with, say, C, then that will be a mutation, because it will change the coding.
Our DNA-synthesizing machinery tends to have an error correction mechanism. It will figure out if there's a problem, usually because the structure is kind of weird; if it's not the right pairing, it will excise and repair the mistake. That happens during replication. It's as if, while you were copying down a text and made typos, you could proofread and fix them. The RNA-synthesizing machinery that most RNA viruses use to copy their genome doesn't have this error correction mechanism. But coronaviruses have a special enzyme that allows them to do error correction, so they have a lower mutation rate than other RNA viruses.
I don't think it works quite as well as the DNA mechanism, though. There's this idea that because most RNA viruses cannot error correct, they make lots and lots of mistakes. That's not great for us, because it allows them to mutate rapidly and avoid the immune system. But if they make too many mistakes, it's not good for the virus either, because the viruses will just break down. And when the replication does make a mistake and it's not caught by the error correction, will the resulting virus be more successful or less successful?
There are three possibilities—mutations can do nothing, they can impair the virus, or they can facilitate the virus replication. If the virus transmits better, then it will more likely be selected [through evolution] to be dominant. If the virus transmits at the same rate, it'll still transmit, but if it's worse at transmitting, it'll get lost.
We've seen in the pandemic that mutations have arisen and then they became really widespread and for almost all of the ones we hear about, it became clear that they have at least slightly better transmission. I don't think it even has to be dramatically better. It just has to have a slight advantage over the original virus. The other aspect is that a virus will make hundreds to thousands of copies of itself every time it is in a cell. The chances of getting a mutant is high just because there's so many replications happening.
Better transmission doesn't necessarily mean that it's more virulent, right? It's just better at replicating and getting into the other cells? Yes, it just means that the initial step of getting into cells is better.
The development of the disease—the pathogenesis—has to do with many other things beside the replication of the virus. Each virus genome is alone, but you can imagine situations where you could have two viruses co-infecting the same cell, and in those cases, they might be able to compensate for each other. There's definitely evidence that some coronaviruses can recombine, too. It there are two genomes that infect the same cell—just like our genomes are combined during the division of the stem cells—they could recombine into a fully fixed genome as it comes out.
Bacteria are giants when compared to viruses. The smallest bacteria are about 0. This makes most viruses submicroscopic , unable to be seen in an ordinary light microscope. They are typically studied with an electron microscope. Their mode of infection is different. Because of their distinct biochemistry, it should come as no surprise that bacteria and viruses differ in how they cause infection.
Viruses infect a host cell and then multiply by the thousands, leaving the host cell and infecting other cells of the body. A viral infection will therefore be systemic , spreading throughout the body. Pathogenic bacteria have a more varied operation and will often infect when the right opportunity arises, so called opportunistic infection. The infection caused by pathogenic bacteria is usually confined to a part of the body, described as a localized infection.
These infections may be caused by the bacteria themselves or by toxins endotoxins they produce. Examples of bacterial disease include pneumonia , tuberculosis , tetanus , and food poisoning. It varies greatly. You need really close intimate contact, blood transfusion or sexual contact.
This coronavirus, by comparison, seems to be relatively stable so that it is able to survive in the environment for hours and maybe a few days, and others are even more stable than that. Polio virus is stable even in sewage—you pick it up by drinking contaminated water.
It passes through the gut, through the stomach, which is almost like pure hydrochloric acid—and the virus is still stable in that.
So some are amazingly tough, and some are quite fragile. Taylor McNeil can be reached at taylor. Skip to main content. A Tufts researcher explains the tiny infectious agents that can wreak havoc globally. Here, an image of an isolate from the first U. The spherical viral particles, colorized blue, contain cross-section through the viral genome, seen as black dots. Photo: CDC. By Taylor McNeil. April 3, Are viruses alive? Viruses mutate and evolve, making them tougher to fight.
The gigantic mimivirus — an example so large that it was initially mistaken for a bacterium, and has a genome larger than that of some bacteria — carries genes that enable the production of amino acids and other proteins that are required for translation, the process that for viruses turns genetic code into new viruses. Mimivirus still lacks ribosomal DNA, which codes for the assembly of proteins that carries out the translation process.
Read more: What happens in a virology lab? Another sign of the fuzzy boundaries between living and non-living is that viruses share a lot of their genetics with their host cells. A study of protein folds, structures that change little during evolution, in thousands of organisms and viruses, found folds shared across all and only 66 that were specific to viruses.
The Royal Institution of Australia has an Education resource based on this article. You can access it here. Originally published by Cosmos as Why are viruses considered non-living?
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