Viruses Or Vesicles

[LeVere]

Extracellular vesicles and viruses: Are they close relatives?

It seems to me that virologists don't want to do the obvious and control for differentiated toxicity(see my other thread with the Korean toxicology paper).

It's obvious that there is not viruses. They talk about the difficulty of separating virions from EVs, the problem is there is no precedent of ANY kind of qualitative separation of a virus clear on back to the very first one TMV. The parsimonious conclusion to draw from the failure of Koch's postulates as well as fulfilling the old electron microscope based protocol which is based on Koch's postulates is that vesicles are all there are and is as far as viral activity goes.

The differentiating factor is clearly stress and toxicity not an exogenous viral agent.

 

[InChristAlone]

Extracellular vesicles and viruses: Are they close relatives?

It seems to me that virologists don't want to do the obvious and control for differentiated toxicity(see my other thread with the Korean toxicology paper).

It's obvious that there is not viruses. They talk about the difficulty of separating virions from EVs, the problem is there is no precedent of ANY kind of qualitative separation of a virus clear on back to the very first one TMV. The parsimonious conclusion to draw from the failure of Koch's postulates as well as fulfilling the old electron microscope based protocol which is based on Koch's postulates is that vesicles are all there are and is as far as viral activity goes.

The differentiating factor is clearly stress and toxicity not an exogenous viral agent.

I've always thought there is something more to viruses than you catch one and makes you sick. But what about Ebola? Rabies? How do we explain how contagious those are? And why is it when a small child goes into the nursery at church in exactly 3 days they get a cold because someone there had a cold?

 

[lollipop]

I've always thought there is something more to viruses than you catch one and makes you sick. But what about Ebola? Rabies? How do we explain how contagious those are? And why is it when a small child goes into the nursery at church in exactly 3 days they get a cold because someone there had a cold?

Good questions @Janelle525 exactly my train of thought. I haven’t heard a good answer yet that explains these two conflicting pieces of evidence.

 

[InChristAlone]

One explanation I heard was that our body can sense when someone is ill and then it like lowers our immunity or something and we 'catch' it.

 

[LeVere]

I've always thought there is something more to viruses than you catch one and makes you sick. But what about Ebola? Rabies? How do we explain how contagious those are? And why is it when a small child goes into the nursery at church in exactly 3 days they get a cold because someone there had a cold?

Well the counter theory is that exoviral disorders are really exotoxin disorders. It's the transference of toxins and stress which induce the release of vesicles. I posted some of the ideas of a poster on questioningaids from 10 plus years ago who had a very convincing explanation for viruses and the different types. Here's his hypothesis on ebola.

Cyanide connects Ebola virus to the mine (ame-g4205)

He has other posts to which you can look up. Some toxicological disorders are acute poisoning processes some are based on long term quantitative toxic stress build up. The point is that differentiated viral processes are explained by differentiated toxicological stress processes.

 

[LeVere]

One explanation I heard was that our body can sense when someone is ill and then it like lowers our immunity or something and we 'catch' it.

I think the factor is that stress can actually be communicated via microbes and other micro organisms and induce endogenous viral responses. You have a source of toxic stress disorder which causes other infected bodies to sound a sort of alarm when they come into contact and communication with this source infected body. This is what explains the viral contagion affect. Eventually the down stream infected bodies figure out that there is no source toxicity and the viral infectious process comes to an end. What's not debatable within germ theory dogma is that infectious cycles DO come to an end and there are really only two explanations as to why viral replication does not go on indefinitely, one explanation I presume is that successive 'immune' responses eventually kill the 'virus', the other explanation is what I just provided. I don't actually entertain the existence of an immune system seeing as I take to Jamie Cunliffe's morphostasis hypothesis and not the immune system hypothesis in regards to disease.

 

[lollipop]

I think the factor is that stress can actually be communicated via microbes and other micro organisms and induce endogenous viral responses. You have a source of toxic stress disorder which causes other infected bodies to sound a sort of alarm when they come into contact and communication with this source infected body. This is what explains the viral contagion affect. Eventually the down stream infected bodies figure out that there is no source toxicity and the viral infectious process comes to an end. What's not debatable within germ theory dogma is that infectious cycles DO come to an end and there are really only two explanations as to why viral replication does not go on indefinitely, one explanation I presume is that successive 'immune' responses eventually kill the 'virus', the other explanation is what I just provided. I don't actually entertain the existence of an immune system seeing as I take to Jamie Cunliffe's morphostasis hypothesis and not the immune system hypothesis in regards to disease.

Very interesting.

 

[LeVere]

It's not hard to figure out if you've read people like Hans Selye and his ideas of stress as a dynamic biological process. Plants for example communicate stress when facing consumed predation. The mimicry replication process is part of evolution and simply manifests itself in things like toxic stress induced contagion.

 

[ecstatichamster]

Extracellular vesicles and viruses: Are they close relatives?

It seems to me that virologists don't want to do the obvious and control for differentiated toxicity(see my other thread with the Korean toxicology paper).

It's obvious that there is not viruses. They talk about the difficulty of separating virions from EVs, the problem is there is no precedent of ANY kind of qualitative separation of a virus clear on back to the very first one TMV. The parsimonious conclusion to draw from the failure of Koch's postulates as well as fulfilling the old electron microscope based protocol which is based on Koch's postulates is that vesicles are all there are and is as far as viral activity goes.

The differentiating factor is clearly stress and toxicity not an exogenous viral agent.

Ironic that Robert Gallo is one of the paper authors, given his role in the misdirection of AIDS research and dishonesty and lack of integrity according to some people whom I respect...

 

[ecstatichamster]

nothing about viruses is straightforward. For instance, very puzzling is the 1917 influenza epidemic. The Navy could not infect most subjects in a major study with flu even innoculating them repeatedly with mucus from flu-stricken people.

I think it was a type of bacterium that was not detected, rather than a virus.

Edgar Hope-Simpson felt that the flu was from vitamin D insufficiency.

On the epidemiology of influenza

The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns." Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify – and attempt to explain – nine influenza conundrums: (1) Why is influenza both seasonal and ubiquitous and where is the virus between epidemics? (2) Why are the epidemics so explosive? (3) Why do they end so abruptly? (4) What explains the frequent coincidental timing of epidemics in countries of similar latitude? (5) Why is the serial interval obscure? (6) Why is the secondary attack rate so low? (7) Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport? (8) Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers? (9) Why has influenza mortality of the aged not declined as their vaccination rates increased? We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. We hypothesize that two factors explain the nine conundrums: vitamin D's seasonal and population effects on innate immunity, and the presence of a subpopulation of "good infectors." If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.
---

'NO HUMAN EXPERIMENTAL STUDIES PUBLISHED IN THE ENGLISHLANGUAGE LITERATURE DELINEATING PERSON-TO-PERSON TRANSMISSION OF INFLUENZA.”

--

they mixed all the “stuff” (secretions from flu stricken people) together and sprayed one cc of the mixture in each of the nostrils of 10 volunteers, and “into the throat, and on the eye” and waited ten days for the volunteers to fall ill. However, “none of them took sick in any way.”

Undaunted, Rosenau conducted another experiment in which ten acutely ill influenza patients coughed directly into the faces of each ten well volunteers. Again, “none of them took sick in any way.”

 

[lollipop]

And there is this:

Is your stress changing my brain?

Is your stress changing my brain? Stress isn't just contagious; it alters the brain on a cellular level

 

[LeVere]

Ironic that Robert Gallo is one of the paper authors, given his role in the misdirection of AIDS research and dishonesty and lack of integrity according to some people whom I respect...

Oh yeah, the irony isn't lost on me. If you look at the perth group stuff I posted their latest communiques include a link to this paper with the question of whether Gallo is slipping from orthodox virology. He obviously doesn't want to conclude the obvious.

 

[SOMO]

The HIV Antibody Test is great for a "YES/NO" answer regarding the person's autoimmune status.

Also Endogenous Retroviruses are probably responsible for "writing" much of our genome.
https://www.pharmaceutical-journal....uman-endogenous-retroviruses/11135043.article

The Central Dogma states DNA -> RNA -> Protein.

But Endogenous Retroviruses prove the Central Dogma wrong because they do Protein -> RNA -> DNA (also called Reverse Transcription.)

Before ERs were proven to do Reverse Transcription, HIV researches said RT was ONLY capable by the HIV virus. Now we know RT is a normal process of animal cells, viruses, retroviruses and most life.

 

[SOMO]

Ironic that Robert Gallo is one of the paper authors, given his role in the misdirection of AIDS research and dishonesty and lack of integrity according to some people whom I respect...

Gallo will take credit for ANYONE else's discovery. He's actually known for it.

This has happened before, now he's trying to butt his way onto the same platform that he denied to people who first talked about Vesicles and Cell Debris.

 

[LeVere]

The HIV Antibody Test is great for a "YES/NO" answer regarding the person's autoimmune status.

Also Endogenous Retroviruses are probably responsible for "writing" much of our genome.
https://www.pharmaceutical-journal....uman-endogenous-retroviruses/11135043.article

The Central Dogma states DNA -> RNA -> Protein.

But Endogenous Retroviruses prove the Central Dogma wrong because they do Protein -> RNA -> DNA (also called Reverse Transcription.)

Before ERs were proven to do Reverse Transcription, HIV researches said RT was ONLY capable by the HIV virus. Now we know RT is a normal process of animal cells, viruses, retroviruses and most life.

I and The Perth Group have some issues with HERVs as well http://www.tig.org.za/PG.Response_to_Martin_Barnes.pdf

 

[LeVere]

Here's some more studies where they continue to reify HIV into their equations. Really all you need to understand is toxicity and stress as far as EVs go. That is clearly the more parsimonious explanation as opposed to these discrete evolutionary viral agents which supposedly are neither alive or dead. Vesicles not Viruses.

Role of Extracellular Vesicles in Viral and Bacterial Infections: Pathogenesis, Diagnostics, and Therapeutics
Hot News: Exosomes as New Players in HIV Pathogenesis - New Data from the IAS 2017. - PubMed - NCBI
Exosomes from uninfected cells activate transcription of latent HIV-1. - PubMed - NCBI

 

[LeVere]

wissenschafftplus.de/uploads/article/Dismantling-the-Virus-Theory.pdf

 

[gaze]

nothing about viruses is straightforward. For instance, very puzzling is the 1917 influenza epidemic. The Navy could not infect most subjects in a major study with flu even innoculating them repeatedly with mucus from flu-stricken people.

I think it was a type of bacterium that was not detected, rather than a virus.

Edgar Hope-Simpson felt that the flu was from vitamin D insufficiency.

On the epidemiology of influenza

The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns." Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify – and attempt to explain – nine influenza conundrums: (1) Why is influenza both seasonal and ubiquitous and where is the virus between epidemics? (2) Why are the epidemics so explosive? (3) Why do they end so abruptly? (4) What explains the frequent coincidental timing of epidemics in countries of similar latitude? (5) Why is the serial interval obscure? (6) Why is the secondary attack rate so low? (7) Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport? (8) Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers? (9) Why has influenza mortality of the aged not declined as their vaccination rates increased? We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. We hypothesize that two factors explain the nine conundrums: vitamin D's seasonal and population effects on innate immunity, and the presence of a subpopulation of "good infectors." If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.
---

'NO HUMAN EXPERIMENTAL STUDIES PUBLISHED IN THE ENGLISHLANGUAGE LITERATURE DELINEATING PERSON-TO-PERSON TRANSMISSION OF INFLUENZA.”

--

they mixed all the “stuff” (secretions from flu stricken people) together and sprayed one cc of the mixture in each of the nostrils of 10 volunteers, and “into the throat, and on the eye” and waited ten days for the volunteers to fall ill. However, “none of them took sick in any way.”

Undaunted, Rosenau conducted another experiment in which ten acutely ill influenza patients coughed directly into the faces of each ten well volunteers. Again, “none of them took sick in any way.”

sorry for bump.

amazing paper, thanks for the share

I know they mentioned equator countries still have it possibly because of sun avoidance, but are there any examples of areas or populations with year round sunlight without any influenza at all that you have seen any research done on?

 

[LeVere]

nothing about viruses is straightforward. For instance, very puzzling is the 1917 influenza epidemic. The Navy could not infect most subjects in a major study with flu even innoculating them repeatedly with mucus from flu-stricken people.

I think it was a type of bacterium that was not detected, rather than a virus.

Edgar Hope-Simpson felt that the flu was from vitamin D insufficiency.

On the epidemiology of influenza

The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns." Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify – and attempt to explain – nine influenza conundrums: (1) Why is influenza both seasonal and ubiquitous and where is the virus between epidemics? (2) Why are the epidemics so explosive? (3) Why do they end so abruptly? (4) What explains the frequent coincidental timing of epidemics in countries of similar latitude? (5) Why is the serial interval obscure? (6) Why is the secondary attack rate so low? (7) Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport? (8) Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers? (9) Why has influenza mortality of the aged not declined as their vaccination rates increased? We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. We hypothesize that two factors explain the nine conundrums: vitamin D's seasonal and population effects on innate immunity, and the presence of a subpopulation of "good infectors." If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.
---

'NO HUMAN EXPERIMENTAL STUDIES PUBLISHED IN THE ENGLISHLANGUAGE LITERATURE DELINEATING PERSON-TO-PERSON TRANSMISSION OF INFLUENZA.”

--

they mixed all the “stuff” (secretions from flu stricken people) together and sprayed one cc of the mixture in each of the nostrils of 10 volunteers, and “into the throat, and on the eye” and waited ten days for the volunteers to fall ill. However, “none of them took sick in any way.”

Undaunted, Rosenau conducted another experiment in which ten acutely ill influenza patients coughed directly into the faces of each ten well volunteers. Again, “none of them took sick in any way.”

There's some really good info in there actually. This is the kind of things that along with other data will take apart the foundational germ theory of disease a theory that does not understand symbiogenesis and does not understand stress as an acute communicable phenomena via toxicity and microbial vectors of given toxicities.

 

[methylenewhite]

I know they mentioned equator countries still have it possibly because of sun avoidance, but are there any examples of areas or populations with year round sunlight without any influenza at all that you have seen any research done on?

I live 600 km from equator. Sun almost all year around. We have at least 3, usually 4 flu-like outbreaks per year. All population affected. Poor and rich, sun avoiders and field workers, all types of genetics backround. It's my personal perception. May be I'm wrong. I had flu-like infections may be 5 times last year. Already had one this year. If you want you can pay me vit D blood test to confirm, would be about 25-30 usd. I'm pretty sure my levels are above 100 ng/mL. I walk and tan a lot. And I'm blonde Caucasian.