One of the things that I find most interesting about viruses is the diversity in their replication cycles. It seems that for every barrier that viruses encounter during replication it is overcome in a myriad of ways.
Imagine you are a warrior invading a castle. How many different ways can you penetrate the defenses, cross the moat, get through the walls, and then access and use all the stuff inside for your own benefit? Will you knock down the gate? Will you sneak through the windows? Catapult yourself over the wall?
A Virus must enter a host cell, take over the machinery to make lots of copies of itself, then get out and transmit to the next host. While the viral replication cycle of all viruses follows the same general patterns, the subtle differences are fascinating. Its like an evolutionary brainstorm that resulted in thousands of different ways to solve the same basic problem.
Ive asked my Biol 105 class to read Ch 19 of Campbell’s Biology and post a comment about an interesting thing about viruses that caught their attention. DId you learn something new and surprising? What is it about it that is interesting to you?
32 thoughts on “Have Fun Storming the Castle!”
Cholera is an excellent example of this…only Vibrio cholerae infected with a prophage cause the severe diarrhea associated with cholera. Diptheria is another good example.
Once integrated there is no actual difference between viral and cellular DNA and genes. Repair machinery and cellular replication machinery cant tell the difference so propahare (or provirus) DNA gets repaired and replicated along with cellular DNA. In fact, the human genome is so heavily populated by remnants of integrated viral genomes that there is more viral DNA than human genes in our own genome!
I was wondering what kinds of information would be contained in the viral genome. And what does it mean to for a virus to “carry a disease?” Are different disease viruses different only in the ways they invade host cells, or are there other disease-specific information that’s contained in the genome? Also, are there different versions of the same virus? (Tuberculosis virus that affects either the eye, or the lungs) Like, would varying the DNA slightly result in a completely different kind of virus, or would it be the equivalent of changing eye color in humans?
I was surprised by how relatively recently viruses have been discovered. I must have been under the false impression that viruses were known about as long as the concept of bacterial infection, yet the original inquiry by Mayer came not even 120 years ago, while the first isolation of a viral particle came only 75 years ago. In perspective, Vassar was founded well before the concept of viruses was even formally cogitated! If anything, this is yet another testament to the exponentially expansive nature of our knowledge of the sciences within the last 150 years.
Prior to reading this chapter, I only knew two things about viruses: that they only possessed some qualities of living things, and that they utilized other cells to reproduce. Therefore, it surprised me when I learned that there was a debate about the origin of viruses and how they evolved. I mean, obviously everything that exists has to originate from somewhere, but since I do not see viruses as living, I was socked to learn the changes and mutations that occurred to allow something that is, to some, not a life form, to adapt to its environment. I was also fascinated by the occurrence of “emerging viruses” that can lie seemingly dormant until they emerge again in a different form or different part of the world. This ability viruses possess is obviously linked to the ability of viruses to mutate and adapt, and is simply fascinating that something with such a simple structure can be capable of such flexibility… and also capable of damaging and infecting so many species worldwide.
After I finished reading Chapter 19, I found myself most interested in Concept 19.2, “Viruses reproduce only in their host cells”. Before reading this, I had a very basic understanding of the lysogenic cycle in which the phage genome of a virus is simply replicated and the host cell is not destroyed, but I was surprised to learn about the lytic cycle. In this case, the host cell is ultimately killed off after the phage injects its DNA, more phages are created and the cell lyses. It fascinated me just by the simple fact that a virus is such a tiny specimen causing such massive destruction on a cell.
What interested me the most was the idea that viruses identify their host cell by a “lock and key” fit and viruses have a host range that can either be very broad or slim. It is interesting to see how viruses, although they are not considered living, have a “mind of their own” and carry out their purpose to reproduce by finding a host cell.
I find it most surprising that a lysogenic bacteriophage can remain undetected for so long within a bacteria. I am curious how these viruses’ genetic code can remain undetected by the DNA repair machinery in the bacteria. Likewise, I am interested in how HIV and proviruses are never discovered by nucleotide repair machinery.
I, for some reason, thought that viruses only really applied to humans. This chapter definitely opened my eyes. I found especially interesting and new the viroids, which can infect plants and kill them too by using the host plant cells enzymes to replicate. I was really shocked to read that ore than 10 million coconut palms in the Philippines were killed by viroids. Its amazing to think of how something invisible to the naked eye can have such great impacts on the world.
One of the first sentences of the chapter really captured much of my amazement about the biological function of viruses, although it was a very introductory statement. The book puts it very bluntly, but to state that viruses exist by injecting their DNA into host organisms, “setting in motion a genetic takeover that recruits cellular machinery to mass-produce more viruses” is a truly incredible discovery of biological science. Even more fascinating is the wide variety of reproductive tactics they have developed, an arsenal made even more impressive by the fact that it is engineered entirely through an evolution that requires host cell machinery. I think one of the most interesting questions to be explored is how viruses, viroids, and prions came into existence, and what kind of influence they have had throughout evolutionary history, especially on eukaryotic organisms (but also bacteria).
I find it so interesting that viruses can invade bacteria–which would otherwise be harmless–and make them potentially life-threatening to humans. I learned from this chapter that the presence of certain prophage genes will cause bacteria to make toxins that, when exposed to humans, make them incredibly ill. I remember learning in the ninth grade that most diseases are caused by either bacteria or viruses. I never considered the possibility of a virus-bacterium combination, which clearly, can be very dangerous.
One thing I found interesting was the fact that viruses are smaller than ribosomes. That such a small particle is able to cause so much damage is amazing. I also thought it was really cool how some phages have a choice whether or nor to destroy their host cell. I would love to learn what kind of environmental signals tell them to switch from the lysogenic to the lytic cycle. The lytic cycle seems much more aggressive.
This technically doesn’t have to do with viruses, but I was really interested by the mention of prions. To think that these even smaller, simpler units are more mysterious and unknown than viruses is strange. I suppose they’re much less frequent and less urgent to respond to than some of the most deadly viruses such as HIV and smallpox, and so there is less incentive to understand them. I think it’s amazing, though, that something so seemingly simple can be ‘incurable’ and unknown.
Although several interesting things about viruses in Chapter 19 caught my attention, prions, or infectious proteins, perhaps awed me the most. Prions are virtually indestructible and have very long incubation periods. They also damage the brain and other neural tissue, which is quite alarming. I did not know that proteins were capable of inflicting such damage. The fact that Mad Cow Disease is caused by prions unnerves me.
I was shocked to find out that viruses, which are capable of killing if not seriously harming entire populations, seem so decievingly harmless. On top of the fact that they are infinitesimally small (some only 20nm in diameter), they are also incapable of reproducing outside of a host (obligate intracellular parasites) and many have narrow host ranges due to the specificity of their viral surface proteins.
I find the simple existence and “attack” of viruses interesting. The fact that these tiny structures have the capacity to just go in and insert their genetic code into another cell fascinates me. In addition, I find the three processes that contribute to the emergence of viral diseases interesting. I am interested to learn more about how viruses can move in between species because when such viruses infect humans, it has a huge impact on our daily lives (i.e. swine flu). Lastly, I was surprised to learn about the “lock-and-key” model. It reminded me of the “lock-and-key” enzyme model.
I was so surprised to discover that, although viruses can carry out all these metabolic processes and have genetic material just like all cells they are not considered cells. This is because they can aggregate into a crystalline shape.This was a discovery of sorts for me because it made these creatures that are so close to the living world are actually even closer to the chemical world than we give them credit for.
Until reading this chapter I was always a little confused as to what limited certain viruses to specific species and why some viruses could easily transfer from one to another. I thought the “lock-and-key” relationship described in section 19.2 did a good job at clarifying that. It sort of goes along with the “storming the castle” metaphor when certain viruses use their surface proteins to infiltrate the receptor sites that hosts initially used to benefit the cell.
I was fascinated by the possibility in viruses’ reproduction of the split between the lytic and lycogenic cycles. I think the most sneaky thing the virus can do is to implant its genetic code and wait a few generations for the actual reproduction to happen. Though obviously it is fantastical to attribute emotions like impatience to viruses, it is cool to think of a virus as completely patient, willing to wait even past its own lifetime to see its progeny come to be.
One thing that I found very interesting about viruses is the idea of how they originated. It is deduced that they had to have originated after cells evolved, since they can only survive within a host cell. The idea that viruses evolved from singular, naked DNA bits that got transferred through different cell membranes is interesting. The evolution of viruses to have membranes and other structures to facilitate entering uninjured cells makes sense, and the continuous, varying evolutionary aspects is natural.
I was most fascinated by the parts of the chapter describing the evolution of Viruses. Just like living things, Viruses change when a random mutant has an advantage in reproducing. A mutated Virus might be harder to detect or might have a wider range of cells that they can infiltrate. This is an amazing process, but also quite frightening. I realized that future strains of Viruses cannot be predicted or prevented. We must first wait for the Virus to come about, and then try and combat it. I dread the day when the HIV virus is albe to pass from person to person with mere contact, or when a Virus similar to Hepatitis is present in the food we eat. However natural selection progresses, there are bound to be new types of Viruses, and as of now, we are somewhat defenseless.
This entire chapter fascinated and interested me, from the lytic and lysogenic cycles and the forms of viral replication, to how a virus identifies their host cell and invades using a “lock and key” sort of method. But what most interested me in this chapter is the retrovirus. The entire conversion and transciption of RNA into two strands of DNA which then is integrated into the host cell’s DNA, and then is replicated as part of the host’s DNA. This is what is so interesting about viruses; they are seemingly biologically inert and have no life about them, but they are capable of such advanced levels of infection and destruction. This is one of many arguments in the ongoing “living or not” debate surrounding viruses.
One thing I found very interesting about viruses is that they are unable to reproduce or make proteins on their own. Although this is the basis of our main argument, I did not have much knowledge of viruses before reading chapter 19. It is so interesting that a simple “packaged set of genes” can cause so much damage to the host it infects. It is hard to believe that viruses have the ability to kill their host cells after using them to replicate and produce proteins necessary to function on their own.
Certainly there are similarities between parasitic bacteria and viruses, however viruses certainly do not fall into a category of bacteria. Viruses are not cellular organisms, whereas bacteria are. Ultimately, we dont even really know where viruses fit into the tree of life. But some strictly parasitic bacteria are totally dependent on infecting a host to survive so there are some “lifestyle” similarities there.
Strictly speaking, prions are not viruses, but rather “infectious proteins”. You have to consume infected material to become infected, such as eating contaminated meat or in cases of the prion disease Kuru, cannibalism is responsible for its spread. So its not like HIV that can be transmitted unknowingly for a long time while the infection goes unnoticed. The biology of prions is fascinating and their discovery led to a Nobel prize.
An interesting thing about viruese that caught my attention is the way in which strains of viruses may be passed on to humans from animals. After reading about a few interactions that happen between strains for them to eventually be able to infect human cells, I initially presumed that the interactions are very complex (which they actually are). However, it seems as though the speed at which interactions and mutations happen, make it apparently easy for viruses to spread from animals to humans.
I quote from page 392, “When an animal is infected with more than one strain of flu virus, the different strains can undergo genetic recombination if the RNA molecules making up their genomes mix and match during viral assembly. Coupled with mutation, these changes can lead to the emergence of a viral strain that is capable of infecting human cells.”
Furthermore, I find it fascinating that scientists or veterinarians opted to “vaccinate birds of several species” to prevent the spread of the H5N1 virus. I understand that this was probably a necessary precaution but nevertheless, I find it very interesting and quite amusing at the same time. This, I believe, of course coupled with the many deaths caused by viruses, shows how serious viral outbreaks can be!
Keeping in mind that I knew nothing about viruses before this, I thought the fact that viruses use another host cell to reproduce to be very interesting. I also found it interesting that viruses are able to infiltrate a cell basically undetected, and use it as a mass producing machine of more viruses. That surprised me because that concept seems so complex. A tiny virus able to take over a cell and integrate its own DNA into the cell’s DNA. This idea leads me into the direction that viruses are alive. Something not living having the ability to take over a living thing doesn’t make sense to me at this time.
After reading Chapter 19, I have come to really appreciate viruses and the ways they function. The most interesting part about the chapter that caught my attention came under Concept 19.3 under the section “Evolution of Viruses.” The section described how viruses may have evolved from both plasmids or transposons and as the text describes, the three are “mobile genetic elements.” They are basically independent from the genome and can act on their own accord. I find it so interesting because I think I’m just used to talking about DNA in its double helix form; hearing more about viruses and their genome is quite surprising.
I found the section on prions to be most interesting because I am fascinated by the brain, and prions can be major threats to the brain. I was very surprised that a prion’s incubation period is at least ten years, because that enormous amount of time allows the virus to be spread unknowingly during that time. Prions are also major threats because they are virtually indestructible and often transmitted through food. It is interesting to have a general understanding of the cause of mad cow disease and why it concerns so many people.
Correction to my statement: A square can be a rectangle but a rectangle cannot be a square. A virus can attack/overpower bacteria, but bacteria cannot overtake a virus. I also found that viruses can attack literally any form of life, plant, fungi and animal.
Before I write my facts of interest..I was thinking. The start of this chapter made me think. A square can be and is a rectangle but a rectangle cannot be a square. Does this apply similarly to viruses, for example do viruses belong as a subcategory of bacteria but it cannot work in reverse? i was just curious because as soon as I saw the comparison of bacteria and viruses, it made me allude to the square and rectangle. But to get back to my facts, I did not know there were two cycles which each played part in surviving by host cell. I was aware that a virus needed a host to survive but did not know about the lytic cycle which ends with the death of the host cell, nor did I know of the lysogenic cycle which replicates the phage genome without killing the host cell. I found the ways of entering the body through the cycles interesting. The line “Phages capable of using both modes of reproducing within a bacterium are know as temperate phages” (phages-capsids found among viruses that infect bacteria) also triggered me to think of the square vs. the rectangle and the virus vs. the bacteria.
What I found fascinating about viruses is that their viral envelopes are derived from the membranes of the host cell, and contain a mixture of host cell and virus proteins. While I was aware that viruses infect cells and modify them, I was not aware that viruses are capable of adopting properties from the host cells to themselves.
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