Home Forums Hunting & Shooting Hunter's Campfire Vaccine resistant strains are here

These doctors can all go fugk themselves.

I was standing in the ER the other day and was handed one by one of those fugking f a g s. I told him it doesn’t fit and he just gave up.

I was standing in the ER the other day and was handed one by one of those fugking f a g s. I told him it doesn’t fit and he just gave up.

I'm just sorry I don't own 10 Chinese mask factories.

Covid is an enhanced more lethal flu, the flu mutates every year just as what they are calling covid is doing. Nothing new about this

King I gotta say I'm more than more happy the wife and I recovered from hopefully the Delta or the latest variant.

Had been using ivermectin as a prophylactic but some Dr.s in the area had reservations about the condom use. They said it works better just after infection. Bummer.

I sincerely believe the Ivermectin kept me out of the hospital and alive.

That said, if I get the crud again I've got a line of a Dr. that will prescribe hydroxychlororoquine with a phone Dr. visit.

Really hoping the Israeli studies pan out. I'll crow when they do.

King I'll bitch at Doc Rocket too.

My sister got the vaxx and she now has covid.

The young man in the linked article below, chose not to be vaccinated & he came down with Covid as well. How is the severity of your sisters Covid?

https://www.keloland.com/keloland-c...n-ventilator-after-contracting-covid-19/

"I have Ivermectin, haven't taken it."

You need to take it now for prevention.

Studies (so far) don't back that up.

Best used at early onset, not as a prophylactic.



D-3, Zinc, V-C are the best preventatives...

Common cold season is back, which has people wondering why we catch the same virus, year after year. Why don't we ever develop immunity against the common cold? Professor Pierre Talbot at INRS has known about the incredible variability of coronaviruses for some time. They're responsible for the common cold as well as many other infections, including neurological diseases. Along with his research associate Marc Desforges, Professor Talbot worked on a study recently published in Nature Communications about the ways in which coronaviruses adapt and evolve, becoming ever more effective at infecting hosts without being defeated by the immune system.

The small, spiky spheres, the coronaviruses are closely monitored by public health agencies, since they're able to be transmitted between species and some have a high potential mortality rate. Both SARS and MERS are caused by coronaviruses. Their ability to adapt to new environments seems due in part to the spikes on the surface of the virus--more specifically, a small, strategic part of the proteins that form those spikes.

The spikes are made up of S proteins (S for spike). A specific part of the spike seems to allow the virus to attach itself to host cells. The spike's RBD (receptor binding domain), which initiates the interaction between cell and virus, is essential for infection. But RBDs are targeted by antibodies that neutralize the virus and allow the immune system to flush it out of the host's system.

Coronaviruses are thus faced with an evolutionary problem. They can't infect cells without an RBD, which needs to be exposed so that it can latch onto cells. But the RBD needs to be masked to avoid being targeted by antibodies.

In response, the coronavirus has developed a mechanism that helps it survive, and thrive. The RBD is made up of three parts that vary widely between strains. Thanks to this variation, antibodies are unable to detect new strains, whereas RBDs retain--and even improve--their affinity for the target cell. Plus, RBDs alternate between visible and masked states.

To gain this insight, a group of researchers including Professor Talbot studied the alphacoronavirus HCoV-229E and, more specifically, the interaction between its RBD and aminopeptidase N (APN)--the host cell protein the RBD latches onto. The team crystallized the multiprotein complex and then analyzed the structures of both proteins.

By observing the RBD's structure up close, the team was able to identify the three long loops that latch onto APN. As analyses of these viruses over the last fifty years have shown, these loops are virtually the only thing that varies from one strain to the next.

The experiments demonstrate that the changes observed in the loops modulate an RBD's affinity with APN. The variants that have the greatest affinity are also likely to be better at infecting host cells, which helps them spread. Six different classes of HCoV-229E have popped up over the years, each with a greater RBD-APN affinity than the last.

This discovery adds to our understanding of the evolution of coronaviruses and could lead to similar analyses of other coronaviruses. Although there are many elements left to explain, the RBD seems to be an important feature that must be monitored as we follow the adaptive evolution of these viruses and assess their ability to infect.

This article has been republished from materials provided by Institut national de la recherche scientifique (INRS). Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference

Wong, A. H., Tomlinson, A. C., Zhou, D., Satkunarajah, M., Chen, K., Sharon, C., . . . Rini, J. M. (2017). Receptor-binding loops in alphacoronavirus adaptation and evolution. Nature Communications, 8(1). doi:10.1038/s41467-017-01706-x

I am not worried because i had the plague and lived.

My system has all it needs to fight this critter.

Until it mutates...............as all coronaviruses do.

Imagine how much money 3M is making.

Do you have any idea how many buildings MANDATE the N-95 right now/?

I think that’s an assumption not supported by the evidence. That is, human’s most certainly have SOME immunity to the common cold, even as it mutates. Just because a virus mutates, doesn’t mean the host loses ALL ability to fight off the infection. Immunity is more than just anti-bodies. There’s also T and B cells and other mechanisms that learn and fight off infections. This is why we have SOME resistance to “new” cold and flu strains, and only get the sniffles or only a fever for a day or two.

If C-19 was such a crafty little devil as to completely evade human immune response in mere months, why has between 40 and 60% of the population immunity due to exposure to “other” corona virus’, and why are SARS survivors still immune more than 15 years later?

I see this becoming an infection that kids get, shrug off, and you might periodically get a cough throughout your life, until your immunity wanes at old age and it does you in. Kinda like pneumonia used to be the “old man’s friend”.