The Virus Page -- Nothing About The Bakken -- February 15, 2020

The coronavirus story has gotten me excited about viruses again. I have a link at the top of the sidebar at the right to the post where I follow this story. I assume I will be able to take down that link by June, 2020, if not earlier. Inshallah.

By the way, just how robust is the United States when it comes to post-graduate education. I've talked about this often. When one speaks of post-graduate education in England, one talks about Cambridge and Oxford. One can throw in Leeds, Edinburgh, and a couple of others, I suppose, Here in the states? Los Angeles, alone, exceeds anything Great Britain has to offer in this arena.

I was reminded of that when it was reported yesterday that "new images of the novel coronavirus were released from the National Institute of Allergy and Infectious Diseases' Rocky Mountain Laboratories in Hamilton, Montana." Hamilton, Montana? Say what. This alone inspires me to want to live forever. What else have I missed? What else will we see in the next fifty years? Graphics pending.

I know nothing about Hamilton -- I've driven through Hamilton -- and I certainly know nothing about the national lab ther.e My hunch is that it came about because of the hysteria surrounding "Rocky Mountain spotted fever" some decades ago. Rock Mountain spotted fever even has its own acronym: RMSF. Any disease with "spotted" in it gets our attention. Likewise, have you noticed that the current coronavirus is often described as the "novel" coronavirus, and its official name will include "novel" to remind us how terrifying this virus was, when we look back at 2020. Hindsight.

Personal note: the very, very, very first patient I ever took care of after getting out of training was a 7-year-old boy with a tick bite recently from Montana .. and the Rocky Mountains. The dad was one of my best friends, a general surgeon, who had just been assigned to Grand Forks AFB, just as I had. He was convinced this son was going to get RMSF. Against my protestations, we put the child on oral chloramphenicol - well known for risk of aplastic anemia. I don't know why we did didn't use doxycycline -- either it was not available or not recommended for children under 7. I don't recall. The patient did fine.

My hunch about history of RML? Correct. See this site. Hamilton is south of Missoula, MT, in one of the most beautiful areas in the world. I don't recall Hamilton but I would have driven through it on one our annual trips to Flathead Lake, also one of the most beautiful areas in the world.

Masks. Surgical asks do not work (by the way, that brings up another issue, but that will have to wait for another day) to prevent coronavirus; surgical masks don't come close to protecting against viruses. The N95 respirators generally don't work either, so that begs the question: why are we not seeing a bigger collapse of the healthcare system in Wahun, or elsewhere for that matter? If you enjoy this stuff, be sure to check out the linked sites. I follow this one. At that site, there are many, many more links. The home site is worldometer.

Dire: Harvard professor says it is likely the "governing" world body will call this a "pandemic" before the year is over. He says 40% to 70% of the world "could" be infected this year.  Proportion of those that will be symptomatic:

"I can't give a good number," he says. 

Or a bad number.

Does a tree falling in a forest make a noise if there is no one there to hear it?

Japan reported an interesting case yesterday: a 50-year-old man in Hokkaido who says he had not recently traveled outside of his local area.. In New Scientist, two reporters wrote that "no one knows if the virus could infect 60% of the world's population and kill 1 in 100 of those infected -- around 50 million people because there are many things we still don't know about the virus."

Right now, the case fatality rate is somewhere between 2 and 3 percent.

So that brings me to Ebola. There was a link over at Drudge about how Ebola might help fight one of our worst cancers -- brain tumors. I didn't care much for the article one way or the other, but it did give me a chance to review Ebola to some extent. This past month I have been reading two books on origin of life, so the review of Ebola was particularly interesting.

First interesting site: how Ebola kills. Kind of amateurish, but it got me started.

A better article over at NIH. Some data points that make this so interesting:

• only primates are susceptible to Ebola
• non-human primates are the intermediate hosts for Ebola -- 2019, J Infect Dis; 
• it is not understood why rodents, rats, for example, are not affected by Ebola
• Ebola: an RNA virus of the Filoviridae family
• the only other member of this family, Marburg, which is just as fatal, but not nearly as "exciting" to the general public
• the virus has only seven genes -- only seven genes -- I find that incredibly interesting -- seven genes
• the seven genes? encode at least eight proteins -- huge data point -- does away with the "one gene-one protein" theory -- and that theory has been with us for decades -- all science is settled for global warming but everywhere else we continue to learn more ... but I digress ..
• case-fatality ratios, early on, 90% in humans and virtually 100% in experimentally-infected non-human primates (NHP) -- compare with novel coronavirus: 2% case-fatality rate (which will probably decrease in time)
• all animal species, equipped with natural barriers to infection, to include, among others:
• cellular sensors
• innate cytokines
• innate immune cells 
• "infectivity" sequence:
• first: the Ebola virus easily, described as a "promiscuous process," easily attached to surface proteins on target cells -- of course that's the most important step for a virus -- finding something to which to attach
• the target cell envelopes the virus and brings it inside the cell, in a little sac, called an endosome; under "normal" circumstances that would be the end of the story, but..
• .. the Ebola virus then engages another receptor inside the endosome -- this receptor / this process is indispensable for Ebola virus infection
• animals (rodents) with mutations such that they don't have this particular receptor are resistant to Ebola infection
• most interesting: animals have different mutations, different genetic protein receptors that give them species-specific immunity: the receptor in that endosome is genetically different in rodents from snakes (Russell's vipers, King cobras) and bats (African straw-colored fruit bats, for example) ... that suggests to me that other species have evolved to survive Ebola and that evolution occurred at the time primates "broke away" from non-primate animals... or primates somehow changed ... after the break ..
• the Ebola virus targets a broad range of primate cells -- epithelial cells, liver cells, and, unfortunately, some cells involved in the immune system, such as macrophages (everyone knows about macrophages) and dendritic cells (something new for me)
• dendritic cells are antigen-presenting cells (also known as accessory cells) of the mammalian immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems.
• dendritic cells are the bridge between innate and adaptive immunity -- dendritic cells are necessary to process pathogens into defined receptors and carry them to T cells that have never seen Ebola before; considering that most of the human population has never seen Ebola virus ("immunologically naive"), the dendritic cell - T cell bridge is incredibly important -- in fact, it looks like this may be the crucial detail in studying Ebola virus
• bottom line: the dendrites do their job picking up the Ebola virus but fail to do anything with the virus before handing it over to the T cell .... "hey, you dendrites .... you had one job to do ...." 
• and, then, of course, it's history, it's too late .. the Ebola virus is inside the human body undetected; 
• the rest of the genes then do the dirty work
• one assumes there are many viruses that have ways, like Ebola, of pranking the human immune system but fortunately don't have the other genes to cause death
• interestingly enough, part of the immune system is to suppress a strong inflammatory reaction when exposed to a foreign particle -- the exception... macrophages .... "macrophages are remarkable exceptions." In these cells, Ebola infection elicits a strong inflammatory response .. and that's what kills us when we get Ebola
• enough of this, time to move on but I have a much, much better understanding of Ebola
• thank you novel coronavirus for piquing my curiosity
• oh, one more thing: the genetic sequence of the seven-gene virus:
  
• under the electron microscope, the Ebola virus looks like a "hangman's noose":