ExtravagantEnzyme

Virulence is defined as causing damage to the host. If the virus kills everyone in that small proximity, the virus will no longer be able to reproduce or spread, plain and simple.

Viruses are super crafty in obtaining their limited number of proteins from the host. However, some viruses bring enzymes with them to get the job done without much help from the host. These are typically larger RNA viruses. Influenza is in this group, but it still steals the 5' cap from the host. This happens without miss as it's able to interact with the host RNA polymerase undetected and then this cap makes it so the influenza RNA appears to be host RNA.

The 1918 influenza was so deadly as it had just jumped to a new host, humans. The same exact influenza responsible for the 1918 pandemic has relatives still in circulation. It's not in circulation as the less virulent versions were more successful. This explicitly demonstrates the preference to be less virulent.

If a virus doesn't need many proteins from the host, it's able to reproduce much more quickly than one dependant on more host resources. The more resources it needs, the increased ability of the immune system to prevent it's reproduction. So in many situations, a lower requirement for host resources can make it more successful. Regardless, it can be very dependent on host resources, like many DNA viruses, and still not be very virulent. A great example of this is Hepatitis D. Virology is a fascinating field and it's highly intricate as a virus is more like it's host than any other viruses. There's not a lot of commonality between different viruses and their reproduction cycles. So viruses in the same family are compared, and the 1918 becoming less virulent shows there's a preference for becoming less virulent over time.

Then why does bird flu have more invasive symptoms and a higher mortality rate compared to human influenza's? I was taught by a virologist who's been around the block many times and got her PhD in the USSR. She was adamant that a parasite never wants to kill it's host, as this results in no longer being able to reproduce in the host and shortens it's reproduction time in future host.

Most viral offspring are not capable of infection, as without mutations, viruses would not be able to reproduce effectively and could not adapt to changing environments. To disprove a hypothesis simply means one aspect of the statement is incorrect. So while the cause and effect occurs, the explanation for why wasn't dialed. Or at least, this would be my guess for how it could have been disproven.

We've known since at least March that about 10 human cases of this new bird flu would allow the virus to mutate and adapt to humans. This is the 14th reported case in the states this year, and the first which could have been transmitted from human to human. We understood what was happening, yet have really done nothing to try to prevent it's spread.

The mutation rate baked into Influenza's reproduction cycle is much more elaborate than coronaviruses, and this isn't exactly a bad thing. When a human catches bird flu from a bird, the mortality rates are pretty burly as this version of the virus attaches to the α2:3 receptor. While this receptor is found throughout the avian digestive and respiratory track, it's only found in the lower lungs of humans. A lower lung infection will always be gnarlier than an upper respiratory infection. Human influenza viruses have a preference for the α2:6 receptor, which is found throughout our airway. This is the primary adaptation which occurs when influenza mutates to infect humans. But a virus is a parasite, so in their ideal world, they wouldn't kill their host. Viruses often do the most damage when adapting to or having recently adapted to a new host. Hopefully, the mutation rate of influenza will result in a shorter pandemic compared to COVID if it ends up taking place.

“Shots fired, into the sky, are now returning, where the fuck will you hide?”

Rise Against — Rumors of My Demise Have Been Greatly Exaggerated

Oh, I see, I interpreted the statement as Mozilla handing over previously collected user data as payment for getting AccuWeather's widget.

However, any webpage visited in a bowser provides this info. So if you haven't stopped it happening from the get, you're handing this data over in mass. But thanks for clearing that up for me!

Why would Mozilla pay AccuWeather in user data? This would cut into their revenue and be horrendous press. Doing so makes no sense, legit entirely illogical. AccuWeather paid to get placement on the new tabs page. But, if you're this worried about it and haven't spent time in about:config to prevent fingerprinting, tracking, and location data collection, start there for sure. Either way, this seems like a huge stretch and wouldn't make sense for Mozilla try and pull off.

Are you implying Mozilla paid AccuWeather to have placement on it's browser? It's always the other way around, think about Google paying to be the default search engine on Safari. If anything, I have to think Mozilla was paid to incorporate AccuWeather and not the other way around.

I mean, cellular/molecular biology is applied organic chemistry. It's all chemical based in some way or another. I guess with T and B cell receptor formations, each receptor binding domain is made totally at random. So much so, they go through training to ensure they won't attack self and are able to detect pathogen associated molecular patterns. Wildly, most T and B cells don't pass training and get recycled, more or less.

So maybe, but you're talking about the world on the cellular level, it's all based on chemical reactions with environmental stimuli. To be alive requires responding to your environment, and chemistry is how that works at the microscopic level.

Immune cells form from stem cells. From start to finish in the stem cell differentiation process, four major changes occur. Some of these changes can have up to four potential outcomes each. Here's a map:

While all cells react to their environment based on environmental stimuli and feedback loops, even bacteria and archaea, this is a great example of cell differentiation. All our cells started as stem cells, but the immune system's continuous and consistent use of the process is very unique. It's also the most elaborate and the image is surface level. Most the end cells pictured here will become more specific. Like there's many different T-cells, even T-cells which change so much they don't meet the classification of being a T-cell. The CD16 T-cell is a great example of this happening.

I feel like this is what you were looking for, but I'm not totally sure.

He's truly phenomenal, basically the Harry Mack of spinning. Their set together is unreal!

https://yewtu.be/watch?v=ggLpFa6CQyU

Marc Rebillet and Thundercat had sets too, plus Hamilton Morris was going to give a lecture. The line up was pretty stacked overall and early bird tickets were $250, which isn't unreasonable for a 3 day festival.

I've spent a good amount of time studying various DNA processes and never once made a connection between i-motifs and clippy. Great catch! lol

The thing is, our cells create these "knots" to make room for enzymes to access our DNA. They're quite common as it's required for DNA transcription + replication, chromosome segregation in cell division, telomere maintenance, and to alter gene expression. Not sure how I overlooked what happens if they form more often than intended. Wild to learn it can lead to cancer, neurodegeneration, and heart disorders! Guess I missed two massive aspects when studying all this, the imapct of DNA forming i-motifs too often, and the resemblance to clippy hahaha.