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DocLightning
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Re: A series of posts about virology

Wed Apr 15, 2020 8:41 pm

StarAC17 wrote:
In theory when you contract the same infection again doesn't the replication of the initial virus have to happen to an extent to alert the immune system of the presence of the virus and then the appropriate antibodies are released to neutralize the virus without the host getting sick again. This can explain why someone could test positive for Covid-19 again but not necessarily going to get sick again. Especially given the long incubation time of covid19.

Is this correct or is the immune system respond even faster and if it does, how? Also can an immune person be an asymptomatic carrier even though they will not get sick for however long the immunity lasts.

[/quote]

Interesting question. So here is a study looking at this question in a different coronavirus called 229E. In this study, they infected volunteers with HCoV-229E and monitored their antibody responses. They found that there was an initial antibody response that faded away by 6-12 months. 12 months later, they rechallenged the volunteers with the same virus and found that all of them became infected again, which was defined by recovery of infectious virus by nasal irrigation on at least one day after the challenge, but only one of them got sick (and only mildly at that). They also found that the duration of the infection was a lot shorter the second time around. So yes, if there is only cell-mediated immunity around in the form of memory T cells, the virus will start to replicate, but it won't get very far before the T cells suddenly come screaming down on it like a pack of wolves and snuff it out. Often, this happens so quickly that the patient doesn't even get sick.

First of all, COVID-19 often makes people much sicker than the other four endemic HCoVs. So we can probably expect that for those who do recover, the immune response will be more robust because that illness is fundamentally caused by an inflammatory response, so more inflammation=more robust immune response (without putting too fine a point on it...there are eleventy caveats to that statement). So my guess is that immunity for people who survived COVID-19 will probably last longer, especially for those who got pretty sick. But for most viruses, symptoms do help with transmission. They may not be *strictly necessary* for transmission, but those symptoms help to increase R0 (R-naught, the average number of people who a sick person will infect). So even if people ultimately *do* get reinfected with SARS-CoV-2, I would expect that infection to be asymptomatic or very mild

And that's a big issue that a lot of people seem to have missed. "Contagious" isn't just a yes/no thing. It's a likelihood. *CAN* someone with no symptoms transmit it? Yes. Are they as good at transmitting it as someone who is coughing and sneezing? Probably not.
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StarAC17
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Re: A series of posts about virology

Fri Apr 17, 2020 4:37 pm

DocLightning wrote:

And that's a big issue that a lot of people seem to have missed. "Contagious" isn't just a yes/no thing. It's a likelihood. *CAN* someone with no symptoms transmit it? Yes. Are they as good at transmitting it as someone who is coughing and sneezing? Probably not.


So this is the big "IF" as it has been reported that Covid-19 can exist in aerosol form with simply by talking or breathing.

While that is less likely to cause transmission than a cough or sneeze if there is truth to it then the people who have recovered and a re-exposed might be able to pass it on as well (they won't get sick themselves) along with the pre-symptomatic and asymptomatic cases.

I must say very interest stuff Doc, thanks for posting.
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Airstud
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Re: A series of posts about virology

Wed Apr 22, 2020 8:43 am

DocLightning wrote:
Some are greasy


Gross.
Pancakes are delicious.
 
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Tugger
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Re: A series of posts about virology

Thu Apr 23, 2020 8:20 pm

DocLightning wrote:
.

Doc,
In my reading I have come across a couple things regarding how an infection's introduction can impact the response:

One is that it could be considered "better" (best word I can think of at the moment) to contract COVID-19 through something like you eyes as via that mode it enters the blood directly and the body reacts directly to that. Versus entering through the lungs where is sets up in the alveoli first, does damage there, multiplies, and then enters your blood stream. This reduces your ability to fight the infection by both reducing lung capacity while you are battling a larger number of virus.

The other is that being exposed to numerous carriers (vectors?) in a short period of time can overwhelm the body's systems faster since more virus can grow and multiply faster. I believe this has also been mentioned with the occurrence of a "cytokine storm" caused by the urgent overwhelming response by the body to multiple detection. And this may indicate that being infected by a single interaction or someone who has a low grade infection, gives the body more time that it needs to build a better resistance to the virus.

Is any of this accurate?

Tugg
I don’t know that I am unafraid to be myself, but it is hard to be somebody else. - W. Shatner
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DocLightning
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Re: A series of posts about virology

Fri Apr 24, 2020 2:47 pm

Tugger wrote:
DocLightning wrote:
.

Doc,
In my reading I have come across a couple things regarding how an infection's introduction can impact the response:

One is that it could be considered "better" (best word I can think of at the moment) to contract COVID-19 through something like you eyes as via that mode it enters the blood directly and the body reacts directly to that. Versus entering through the lungs where is sets up in the alveoli first, does damage there, multiplies, and then enters your blood stream. This reduces your ability to fight the infection by both reducing lung capacity while you are battling a larger number of virus.


Not for this virus. The last place you want it is in the blood. That seems to set you up for the clotting stuff we've been hearing about it. I think that for this virus, if you're going to get it, the best place to get it is in your stomach. That's a mucosal surface but it's not going to cause lung issues. The trouble is that of course the GI tract and the respiratory tract cross at the throat, so if you get it in your GI tract, you're going to get it in your respiratory tract.
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einsteinboricua
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Re: A series of posts about virology

Fri Apr 24, 2020 3:58 pm

DocLightning wrote:
The trouble is that of course the GI tract and the respiratory tract cross at the throat, so if you get it in your GI tract, you're going to get it in your respiratory tract.

That's where a Clorox tablet comes in, right? :duck:
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DocLightning
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Re: A series of posts about virology

Fri Apr 24, 2020 11:01 pm

einsteinboricua wrote:
DocLightning wrote:
The trouble is that of course the GI tract and the respiratory tract cross at the throat, so if you get it in your GI tract, you're going to get it in your respiratory tract.

That's where a Clorox tablet comes in, right? :duck:


Yup! Try it and report back to me with results. :angel:
-Doc Lightning-

"The sky calls to us. If we do not destroy ourselves, we will one day venture to the stars."
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einsteinboricua
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Re: A series of posts about virology

Sat Apr 25, 2020 3:48 am

DocLightning wrote:
Yup! Try it and report back to me with results. :angel:

This is not a game!
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DocLightning
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Re: A series of posts about virology

Sat May 02, 2020 3:34 am

The Coronavirus is mutating.
(Well, of course it is!)

Birds fly, fish swim, and viruses mutate.

In each infection, a relatively small population of individual virions (perhaps a few tens to a few hundred, or as few one or two for ebolavirus) infect an individual organism. The virus then reproduces to high copy numbers. Viruses mutate at different rate. Single-Stranded RNA viruses have some of the highest mutation rates with a substitution mutation occurring at 1/10^4-5 nucleotides per cycle (substitutions/nucleotide/cycle, or s/n/c) Consider that a typical ssRNA virus genome might be only 10,000 bases long, that means that there will be a mutation that occurs in somewhere between every replication cycle to every ten replication cycles!

Most of these mutations are bad for the virus. They might change an amino acid in a protein and make it not work as well. Also, in many RNA viruses, the viral RNA itself can fold into specific shapes that affect the viral replication mechanisms (a single base mutation in poliovirus makes it into the vaccine strain and that mutation changes a 3d shape made by the viral RNA during replication), so a change in a single base can affect the virus in that manner, as well.

Because it is so likely that a mutation will be bad for the virus, RNA viruses cannot be larger than 10-15,000 bases or the risk of having two mutations in each virus gets too high and the virus would not be viable.

But as long as that mutation rate is within the range that a virus of a given genome size can tolerate, it can afford for the majority of mutations to be deleterious because a viral infection produces such an enormous number of viral offspring.

The exception to this error rate in ssRNA viruses is the order Nidovirales, of which the family Coronaviridae are a member. Coronaviruses have very large genomes and this rate of mutation would not be sustainable and so their RNA polymerase has an error-correcting function that is pretty unique to RNA viruses. This allows for a much larger genome (about 30,000 bases). Coronaviruses have a mutation rate of about 1/10^6 s/n/c, 10-100 times lower than their other ssRNA brethren.

But the thing to understand about viruses is that VIRUSES ARE ALWAYS MUTATING...or they are not replicating.

"A [virus] population is in a dynamic equilibrium with viral mutants arising at a high rate on the one hand, and being strongly selected against on the other. The genome of [the virus] cannot be described as a defined unique structure, but rather as a weighted average of a large number of individual sequences."
-E. Domingo, D. Sabo, T. Taniguchi, C. Weissman. 1978, Nucleotide sequence heterogeneity of an RNA phage population. Cell 13:735-744


This mutant "cloud" of viral genomes defines a "quasispecies." When that "cloud" jumps from one host to the next, only one droplet (literally) of that "cloud" containing only a small sample of that infection is transferred, so the founding population in each newly infected person is slightly different.

On top of this, there are various selections for and against certain mutations occurring at multiple levels of complexity. One mutation might increase the viral replication rate at the cellular level. This might seem very advantageous for the virus, but if it kills its host too quickly, then this mutation might result in an evolutionary dead-end for the virus (and the host!) because the virus will not be able to spread effectively to other hosts. By contrast, a mutation that makes the virus replicate too slowly might enable the host to completely eradicate the infection before it has the chance to spread, so there is an optimum for each viral property.

So the mutation rate can be affected by the error rate of the polymerase, the selective pressures placed on each nucleotide in the genome, and other events such as deletions and recommendations that can occur during viral reproduction.

So when the media breathlessly reported that there were now 33 strains of SARS-CoV-2, they were wrong. There are a lot more than that. But the selective pressures on the virus keep certain important portions stable, like the receptor-binding domain of the spike protein, which is the bit that we need to make antibodies against.

So the claim that a virus is mutating sounds to me a bit like someone reporting as a front-page headline that "The Earth is Turning Today."
-Doc Lightning-

"The sky calls to us. If we do not destroy ourselves, we will one day venture to the stars."
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DLFREEBIRD
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Re: A series of posts about virology

Sun May 03, 2020 11:44 pm

https://www.nytimes.com/interactive/202 ... tions.html

here is an article about the virus mutating, I am a visual learner, so it really helped my understanding after reading this thread.
again thank you for posting good Dr.
 
agill
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Re: A series of posts about virology

Mon May 04, 2020 2:08 pm

Great post. Was in molecular biology many years ago so a nice refresher.

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