4 ms·

Pity I only get 1 upvote. I'd triple-click if I could. This animation enables one to visualize a single SARS-CoV-2 virion binding with the ACE2 enzyme, enterin

Pity I only get 1 upvote. I'd triple-click if I could. This animation enables one to visualize a single SARS-CoV-2 virion binding with the ACE2 enzyme, entering the host cell, and replicating 4-5 new virions. One SARS-CoV-2 virion is 125 nanometers wide. By the time it shows up on a CT scan we are talking many, many billions. It's seems impossible anyone could test positive and still be asymptomatic.

waterhouse 7y ago
I note that the virus depicted in the animation is HIV. How much of the lifecycle is different from HIV to SARS-CoV-2? One thing I noted is that it said the inserted viral DNA might remain dormant for years; surely that part is HIV-specific? (Or do we really bear viral infections for years after recovery, and—I presume—rely on the continued presence of antibodies to quash the remaining DNA?)
- mardifoufs 7y ago
  That part is mostly specific to retroviruses and DNA viruses. Retroviruses are special because even though they are RNA based they can "translate" their RNA into dna once inside the cell and embed that DNA into the cell's genome. That translation in itself is remarkable since it's the opposite of the normal DNA to RNA "translation" we see in almost every organism, hence the "retro". DNA based viruses don't have that unique mechanism but the result is conceptually the same: you get a virus that is extremely hard to completely cure/remove due to it being present in some of your own DNA. Herpes is a DNA based virus and that's why you can't ever be fully cured from it. That's also why retroviruses like HIV can only be suppressed. It's also why antiretroviral drugs try to inhibit the replication phases of the virus, which makes managing the disease possible but can't remove the virus itself. Still, a cocktail of those inhibitors is an amazingly powerful treatment against AIDS and leads to HIV becoming basically dorment in the body. A ribovirus (which is what coronaviruses are) is RNA based but it doesn't embed itself into our genome. It never translates it's RNA and since RNA is fundamentally less stable of a molecule than DNA, you get really high mutation rates. That "instability" is caused by the lack of a built in error checking mechanism in RNA. Those random mutations are part of why Influenza is hard to build immunity against. But it's also why RNA based viruses are generally either too virulent and mortal to allow for effective spread, or rapidly evolve towards less lethal forms. Keep in mind that I've generalized a lot and that there are a lot of exceptions and outliers when it comes to viruses. For example, Hepatitis C is a ribovirus but it has a special protection mechanism that protects it's core genetic material from mutations even if it's RNA based.
  - nullc 7y ago
    > It never translates it's RNA and since RNA is fundamentally less stable of a molecule than DNA, you get really high mutation rates. That "instability" is caused by the lack of a built in error checking mechanism in RNA. The coronovirues have a proofreader mechanism, which is interesting. And influenza has more potent evolved countercountermeasures than just high mutation rates: https://en.wikipedia.org/wiki/Antigenic_shift https://en.wikipedia.org/wiki/Antigenic_shift
    - mardifoufs 7y ago
      Yep! That's what really makes influenza special, as I said the mutation rates are only part of why Influenza viruses rapidly change. Their ability to cross between species by combining easily with other types of influenza viruses are the key to their incredible variability One of the distinguishing trait of CoVs are their special RNA replication/transcription mechanisms that results in less errors, which is really important considering the large size of their genomes compared to other RNA based viruses. Though, and correct me if I'm wrong, aren't they still extremely less stable than DNA viruses? Which is why only short/medium term immunity is usually possible? I don't know a lot about the synthesis of coronavirus RNA but it looks super interesting
      - nullc 7y ago
        > Though, and correct me if I'm wrong, aren't they still extremely less stable than DNA viruses? That's correct. Worse, the proofreader doesn't have to protect all parts equally... > Which is why only short/medium term immunity is usually possible? No. For some viruses active immunity just doesn't last particularly long for reasons we don't understand (or at least it was described as not understood in every paper I've seen on the subject). For some viruses you can be reinfected months later with exactly the same virus. This is the case for several cold causing viruses.
usrusr 7y ago
> It's seems impossible anyone could test positive and still be asymptomatic. Why? Most symptoms are part of the body's response switching into overdrive and not a direct consequence of cells getting subverted into virion farms. If the immune system wins without resorting to state of emergency measures like a fever you won't notice, but in the meantime there is a phase of viral replication in the throat. With SARS-Cov-2 there is even the pattern that detection drops already in the throat of patients that still have a pneumonia raging in their lung (probably because the throat, as a battlefield in this war, somehow favors the immune system more than the lung?), so it's not even a subset/superset relation between symptoms and positive throat PCR, it's a partial overlap.
- johnohara 7y ago
  Seems impossible but from observation obviously is not. Comorbidity is the issue with SARS-CoV-2. It is interesting that some patients testing positive report losing the sense of taste and/or smell while others report digestive problems prior to the onset of acute respiratory problems or even sore throat.

waterhouse 7y ago

I note that the virus depicted in the animation is HIV. How much of the lifecycle is different from HIV to SARS-CoV-2? One thing I noted is that it said the inserted viral DNA might remain dormant for years; surely that part is HIV-specific? (Or do we really bear viral infections for years after recovery, and—I presume—rely on the continued presence of antibodies to quash the remaining DNA?)

mardifoufs 7y ago
That part is mostly specific to retroviruses and DNA viruses. Retroviruses are special because even though they are RNA based they can "translate" their RNA into dna once inside the cell and embed that DNA into the cell's genome. That translation in itself is remarkable since it's the opposite of the normal DNA to RNA "translation" we see in almost every organism, hence the "retro". DNA based viruses don't have that unique mechanism but the result is conceptually the same: you get a virus that is extremely hard to completely cure/remove due to it being present in some of your own DNA. Herpes is a DNA based virus and that's why you can't ever be fully cured from it. That's also why retroviruses like HIV can only be suppressed. It's also why antiretroviral drugs try to inhibit the replication phases of the virus, which makes managing the disease possible but can't remove the virus itself. Still, a cocktail of those inhibitors is an amazingly powerful treatment against AIDS and leads to HIV becoming basically dorment in the body. A ribovirus (which is what coronaviruses are) is RNA based but it doesn't embed itself into our genome. It never translates it's RNA and since RNA is fundamentally less stable of a molecule than DNA, you get really high mutation rates. That "instability" is caused by the lack of a built in error checking mechanism in RNA. Those random mutations are part of why Influenza is hard to build immunity against. But it's also why RNA based viruses are generally either too virulent and mortal to allow for effective spread, or rapidly evolve towards less lethal forms. Keep in mind that I've generalized a lot and that there are a lot of exceptions and outliers when it comes to viruses. For example, Hepatitis C is a ribovirus but it has a special protection mechanism that protects it's core genetic material from mutations even if it's RNA based.
- nullc 7y ago
  > It never translates it's RNA and since RNA is fundamentally less stable of a molecule than DNA, you get really high mutation rates. That "instability" is caused by the lack of a built in error checking mechanism in RNA. The coronovirues have a proofreader mechanism, which is interesting. And influenza has more potent evolved countercountermeasures than just high mutation rates: https://en.wikipedia.org/wiki/Antigenic_shift https://en.wikipedia.org/wiki/Antigenic_shift
  - mardifoufs 7y ago
    Yep! That's what really makes influenza special, as I said the mutation rates are only part of why Influenza viruses rapidly change. Their ability to cross between species by combining easily with other types of influenza viruses are the key to their incredible variability One of the distinguishing trait of CoVs are their special RNA replication/transcription mechanisms that results in less errors, which is really important considering the large size of their genomes compared to other RNA based viruses. Though, and correct me if I'm wrong, aren't they still extremely less stable than DNA viruses? Which is why only short/medium term immunity is usually possible? I don't know a lot about the synthesis of coronavirus RNA but it looks super interesting
    - nullc 7y ago
      > Though, and correct me if I'm wrong, aren't they still extremely less stable than DNA viruses? That's correct. Worse, the proofreader doesn't have to protect all parts equally... > Which is why only short/medium term immunity is usually possible? No. For some viruses active immunity just doesn't last particularly long for reasons we don't understand (or at least it was described as not understood in every paper I've seen on the subject). For some viruses you can be reinfected months later with exactly the same virus. This is the case for several cold causing viruses.

usrusr 7y ago

> It's seems impossible anyone could test positive and still be asymptomatic. Why? Most symptoms are part of the body's response switching into overdrive and not a direct consequence of cells getting subverted into virion farms. If the immune system wins without resorting to state of emergency measures like a fever you won't notice, but in the meantime there is a phase of viral replication in the throat. With SARS-Cov-2 there is even the pattern that detection drops already in the throat of patients that still have a pneumonia raging in their lung (probably because the throat, as a battlefield in this war, somehow favors the immune system more than the lung?), so it's not even a subset/superset relation between symptoms and positive throat PCR, it's a partial overlap.

johnohara 7y ago
Seems impossible but from observation obviously is not. Comorbidity is the issue with SARS-CoV-2. It is interesting that some patients testing positive report losing the sense of taste and/or smell while others report digestive problems prior to the onset of acute respiratory problems or even sore throat.