Posted on 08/10/2014 12:46:23 AM PDT by Smokin' Joe
I have spent a little time compiling links to threads about the Ebola outbreak in the interest of having all the links in one thread for future reference.
Please add links to new threads and articles of interest as the situation develops.
Thank You all for you participation.
Cold kills cells by slowing chemical processes below viable levels, and by ice rupturing cell walls.
A virus outside a cell has no active metabolism, and is not destroyed by ice formation.
If Ebola ever infects a promiscuous homosexual man in the US, it will spread through the whole gay community within a month.
It was the Senegalese WHO doctor.
He was the one who missed out on the ZMapp because the Brit apparently received the last dose, IIRC.
No it wouldn't be hard.
The suicide infector doesn't need to himself be infected with Ebola. All the suicide infector needs is access to a symptomatic Ebola patient. Get his blood, or other bodily fluid, and smear it on surfaces where lots of people will come into contact with it. The spreader will eventually get it, but by that time he will have been able to contaminate a LOT of places.
I think that last sentence is why our gov’t finally started to pay attention to the outbreak. I imagine someone had to kick the ditherer-in-chief’s backside. That someone could have been CDC Director Friedman, who just experienced a wake-up call from his recent visit to Ebola hell in West Africa.
I stumbled across this slide presentation from a post-doc named Amy L Hartman who spent time at the CDC. I haven't researched her specifically but found slide number 15 of her presentation very interesting.
Ebola Virus Pathogenesis: Lessons learned from my post-doc experience at CDC
Notice the "early symptoms" of Ebola. Cough.
I also ran across a good summary of the virus' replication and transcription process. While reading this struck me:
Filovirus replication and transcription(Future Virology Mar 2007 via NIH)(Pg 2) Filoviruses encode seven structural proteins (Figure 1B & C). While five of these proteins, the nucleoprotein (NP), the viral proteins (VP) 35 and 40, the glycoprotein (GP) and the RNA-dependent RNA polymerase (L) are counterparts of proteins found in all NNS RNA viruses, VP24 appears to be unique to filoviruses, and a protein similar to VP30 is only described for the pneumoviruses [8].
(Pg 6)Besides its function as a transcription activator, EBOV VP30 is involved in nucleocapsid assembly by binding to NP-derived inclusion bodies [21]. VP30 is a P that contains a zinc-binding domain and forms hexamers [57–60]. Phosphorylation of VP30 is presumed to be an important regulatory factor by determining whether the protein is involved in transcription activation or assembly [57].
(Pg 7) Besides filoviruses, the only other NNS RNA viruses possessing a fourth nucleocapsid protein are the pneumoviruses. The fourth nucleocapsid protein of respiratory syncytial virus, M2–1, acts in a later stage of transcription as a processivity factor [49].
Things that make me go, "hmmmmmm." A novel protein involved in the Ebola nucleocapsid that is approximated only by pneumoviruses (viruses that cause respiratory infections).
Maybe I just think too much.
Second thread.
A nagging thought has been flitting back and forth in the back of my brain. So here are some stupid questions.
If Zebola is assumed to spread solely through human to human fluid contact and we are warned not to touch mouths, noses, and eyes where is its micro point of attack? How does it reach the blood stream where its real attack and propagation begin? Through mucosa?
And furthermore, while not defined as a respiratory disease, has the path through the pulmonary system, where vital gas exchange occurs oxygenating the blood, been eliminated as a major avenue of attack? Need lungs necessarily become congested upon viral attack? If the primary goal of Ebola is to reach blood cells can the pulmonary system be considered merely a transit point?
All this is a roundabout way of asking by what route does the Zebola virus reach its goal?
Wow.
That’s probably what Reston mutated around enough to become airborne.
Would be instructive, maybe, to do a folding run with those sequences to see how closely the pneumovirus sequences fold with respect to the reston with respect to zebola. And see if any critical mutations are responsible for any differences/similarities. Or just compare any ‘rcsb’ like data on them. If any exists. And then do a timeclock to see how often that mutation might happen based on Reston vs. other ebola strains.
Imagine what will happen with the DNA of Ebola once it hits the flu season! That collision will produce yet another so called strain.
https://in.news.yahoo.com/netherlands-evacuate-two-doctors-had-contact-ebola-victims-101916632.html?
“Netherlands to evacuate two doctors who had contact with Ebola victims”
Link snagged from the other site. Note that the doctors managed to cross the border into Ghana while potentially already infected with zebola. Mmmm, corruption in Africa...
They aren’t similar enough for that.
What MAY happen is that the symptoms of flu mimic those of ebola early on. And lots of ebola positive people will show in the ER and their doctors offices thinking they just have the flu. And infect the doctors, who if not wearing PPE for every single patient, will be playing roulette. And leave fomites all over the waiting rooms and bathrooms for any subsequent patients to encounter.
They will also be coughing and sneezing and sweating a lot. And if infected concurrently with both of them will become REALLY EFFICIENT ebola spreaders.
p.s. Does not include ebola cases in the Congo.
I have no doubt of that. The treatment centers are full up and turning people away. People who are ebola positive but never recorded as such. People who then return to their families (via taxi!) and subsequently infect them.
Right about the recombination. And the problem with not being able to discern between Ebola and other diseases when symptoms begin to present is going to wreak havoc.
http://www.nytimes.com/2014/09/13/world/africa/ebola-who-africa.html?
“Ebola Outpaces Global Response, W.H.O. Says”
“A surge of 400 new cases in Liberia in the past week, double the number of new cases in the preceding week, was “a particular cause for concern,””
Ya know, with the possibility of transmission of disease prior to a positive test, I’m not sure I would be comfortable in the middle of an outbreak if the MD’s didn’t change PPE after every patient. Would you want to be treated by a doc wearing a PPE they’d been wearing since that morning knowing it only took 1-10 virons to establish infection? And even one patient they’d treated prior to seeing you was infected and just waiting on a positive test for that.
How would the MD differentiate between that and just ordinary flu? They couldn’t. So they’d have to change PPE after every symptomatic patient. For any patient running any fever, with any other symptoms like runny nose, vomiting, coughing. Anything other than normal temp with no symptoms of anything at all.
And even then, if they were an OB/gyn or urologist you could never be certain that the asymptomatic patient hadn’t had a mild case and was still infectious through semen or vaginal fluids so you’d have to do that for every single patient.
Bkmk
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