The e-mails all asked the same questions and they were all about Mother Abigail. Did I know her? Who did she work for? Had I met her? Basically the same e-mail over and over again.
This pretty much let all the wind out of my sails for quite a while. Because the truth is that I knew nothing of her – had exchange a couple of brief “web-based” e-mails and although I had read every word she had ever written on the subject, my knowledge of the person was ZIP.
The only consistent trait of my personality, as several of my ex-wives will tell you, is that I have no great fidelity to any concept. So I fell back and reviewed my goals.
After a season of Tanqueray and tonic I decided to change my focus.
2008
Via e-mail I asked MA if she would be willing to allow me to interview her and write an article about her. My operating paradigm at that time was that this lady was a seminal pioneer of the New Media and a scientist of serious reputation.
How naïve I was.
In the late summer of 2008 I was invited to visit her at her home on Lake Tahoe. It was a visit that would change my life.
DISCLAIMER
The following is a summary of conversations that occurred from August 2008 until June of 2009. All the words are mine and mine alone. When I asked MA if she would like to edit my work or review it for errors – she declined. Prior to the final draft I asked MA for a quote and she declined but requested that I include her favorite poem which I did.
This first part of the interview is hundreds of posts long and is one of the most detailed scientific discussion of influenza (and a lot of other stuff) that you will ever see.
That being said, I believe it to a very interesting read and a rare insight into an exceptionally unique and gifted person.
Here is the direct URL: (You will need to be registered because this discussion was not on the public forum – but in the scientific discussion area).
Enjoy
Mother Abigail Interview Part #1
INTERVIEW WITH MOTHER ABIGAIL PART #2
October 19th, 2009
3. How has her previous work held up to peer review
2003
Her work with SARS speaks for itself. Not only did she create a new media device for information exchange, but her guiding help with health care workers during those troubling days is much commented on in the threads cited above.
2004
In 2004 Mother Abigail, whose life work was with hemorrhagic fever, gave the following analysis of Ebola research. Where she pointed the finger at fruit bats as the reservoir species.
_______________________________________________
Just a quick synopsis of the current state of Ebola research.
GENETIC ANALYSIS OF THE OUTBREAKS
Investigations into the outbreaks of Ebola in humans during the late 1990’s pointed to a link with great apes.
The origins of many of these epidemics could be traced to direct human contact with dead chimpanzees or gorillas, either through hunting bush meat or from handling carcasses found in the forest.
The index [first] cases were mainly hunters and transmission occurred by direct person-to-person contact.
We have identified at least 10 separate chains of transmission, each originating from one index case occurring between October 2001 and May 2003.
By analyzing the genetic material of the virus to see whether these outbreaks had resulted from multiple introductions of a single viral strain or separate introductions of several strains of Ebola it was discovered that:
(1) There were at least eight different strains of Ebola involved, showing that for this relatively short period under study the mode of transmission of the disease was more complex than previously imagined.
(2) Because Ebola is a genetically stable virus - unlike say influenza, which mutates rapidly - the fact that many strains are involved suggested that there have been multiple independent introductions of the virus from the reservoir species into apes and humans.
Different strains of Ebola virus may be widespread throughout the forests of central Africa, with simultaneous infection of great apes occurring from unknown natural hosts under particular but unknown environmental conditions.
Ebola outbreaks probably do not occur as a single outbreak spreading throughout the Congo basin as others have proposed but are due to multiple episodic infection of great apes.
THE UKNOWN RESERVOIR
The great unknown, of course, is the name of this reservoir species.
We aren’t near to identifying the animal but we have some ideas, in particular fruit bats.
We don’t have much evidence at all, just observations and ideas.
Both apes and fruit bats eat the same kind of food so it is not unreasonable to assume that they may come into close contact with one another at certain times of the year.
Ebola outbreaks in wild animals seem to occur at the beginning of the dry season. But no one has yet shown that it is possible to find Ebola virus in wild bats.
In South Africa a scientist succeeded in infecting fruit bats experimentally and he observed rapid development of the virus.
So although it is technically possible to infect fruits bats with Ebola, there is still no evidence that this is the mystery reservoir species.
Until this animal is found, the sole measure that we can take in predicting and preventing an Ebola outbreak in humans is to watch what is happening to gorillas and chimpanzees in the wild.
I wish there were better news.
57 posted on Monday, April 26, 2004 8:05:52 PM by Mother Abigail
http://www.freerepublic.com/focus/ch...=1&;page=51#57
2007
Then in 2007 she names genus and species of the reservoir species.
What concerns me most is that we might begin to see an infection pattern with Ebola that is now well documented in Marburg outbreaks.
1. We know that human infection with Ebola comes about through the intermediary of infected great ape carcasses.
2. The viral transmission to primates occurs in the dry season, a period when food resources become increasingly scarce. The great apes then come into competition with bat species for fruit supplies when foraging and can be infected notably by blood or by placental fluid that escapes when bats give birth. (See my post #57 from 2004)
3. The mode of contamination by Marburg virus appears to be different, however. It does not appear to need any intermediary to be pathogenic for humans, as foreseen from the data on Marburg epidemic outbreaks.
In one outbreak, which raged in the north-east of DRC in 2000, most people infected worked in a goldmine, which turned out to be the refuge for a large colony of Egyptian rousettes. During the second epidemic, in Angola, the first victims were children who had gathered fruit from trees where a large population of this species of fruit bat roosted.
4. R. aegyptiacus - Carries both antibodies and viral RNA fragments - strongly suggesting that this bat species is a non-symptom developing carrier of the Marburg virus - (i.e.) the natural reservoir.
MA
75 posted on 10/09/2007 7:58:39 AM PDT by Mother Abigail
http://www.freerepublic.com/focus/ne...posts?page=6#6
This hypothesis of Mother Abigail was proven true in 2009.
EBOLA AND MARBURG HEMORRHAGIC FEVER, EGYPTIAN FRUIT BAT - WEST AFRICA
************************************************** *******************
A ProMED-mail post
ProMED-mail is a program of the
International Society for Infectious Diseases
Date: Fri 2 Oct 2009
Source: Bloomberg.com [edited]
Virus Hunters Find Ebola, Marburg Source in Fruit Bat
The study, based on blood tests on more than 2000 bats in Gabon and
the Republic of Congo, will help scientists solve a mystery that has
confounded them for more than 30 years: which species harbor Ebola
and Marburg [viruses] without getting sick. The answer may explain
how the viruses persist in the environment and point to ways humans
can avoid a disease that causes fatal bleeding and organ failure in
at least half of cases.
“Very eminent scientists have been searching for decades to find the
source,” said John Mackenzie, a Melbourne-based virologist who
assists the World Health Organization in its response to outbreaks.
“Until you know what it is, you can’t piece together the epidemiology
or begin to think about managing the risks to both humans and wildlife.”
Marburg hemorrhagic fever was recognized in 1967, when outbreaks
occurred in laboratories in Marburg and Frankfurt, Germany, and in
the Serbian [Yugoslavian] capital, Belgrade. Cases were traced to
African green monkeys imported for research and polio vaccine
production. Then, 9 years later, a closely related virus was found to
have sparked a deadly outbreak near the Ebola River in the Democratic
Republic of Congo, formerly known as Zaire.
Disease trackers have tested everything from snakes to guinea pigs in
the search for an animal reservoir and have been repeatedly led back
to caves, mines and bats. A 2005 study published in the journal
Nature found evidence of symptomless ebolavirus infection in 3
species of fruit bat in West Africa, indicating that these animals
may be the ones silently harboring the virus. In March [2009],
scientists reported the 1st evidence directly connecting a human
Ebola hemorrhagic fever outbreak to the putative fruit bat reservoir.
The study reported this week is the 1st to show that ebolavirus and
marburgvirus are circulating simultaneously in bat populations in one
country. While several human Ebola hemorrhagic fever outbreaks have
occurred in Gabon, no cases of Marburg hemorrhagic fever have been
reported there, the authors said. The presence of marburgvirus in the
West African nation represents a “potential and previously
unrecognized threat to humans,” they said.
“These findings provide much stronger evidence for a reservoir in
bats,” Xavier Pourrut, a virologist at Gabon’s International Center
for Medical Research in Franceville and the study’s lead author, said
in a telephone interview. “The next step is to understand how the
viruses circulate in bat populations over time.” Pourrut and
collaborators from the Special Pathogens Branch of the Centers for
Disease Control and Prevention in Atlanta and France’s Institute for
Development Research looked for evidence of previous ebolavirus and
marburgvirus infection in the blood samples of 2147 bats from at
least 9 species. Tests were conducted from 2003 to 2008 in 3 regions
of Gabon and in the Ebola epidemic region of north Congo.
Of all the bats sampled in significant numbers, only specimens of the
cave-roosting Egyptian fruit bat, or _Rousettus aegyptiacus_, were
found to harbor antibodies against both ebolavirus and marburgvirus,
the authors wrote, “suggesting that this species may be a natural
host of both viruses.” The Egyptian rousette, with a doglike face and
ears, is found along the Nile River in Egypt, across Sub-Saharan
Africa, eastern Mediterranean and the Middle East. While some groups
may occasionally roost outside in trees, the bats of this species
prefer to inhabit caves, mines and tombs, and feast on fruit trees at
night. These preferences give it a stronger link with the circulation
of ebolavirus and marburgvirus more frequently found in rain forests,
said Pierre Formenty, leader of the emerging and dangerous pathogens
team at the World Health Organization (WHO) in Geneva.
Formenty was among 29 authors of a study published in July [2009]
that showed Marburg virus could be isolated from seemingly healthy
Egyptian fruit bats caught in Uganda’s Kitaka Cave, where miners
infected with the virus in 2007 had worked. While some outbreaks in
humans have been directly linked to contact with bats, more evidence
exists to link cases with infected apes, chimpanzees and other
primates that are often consumed in Central Africa. These animals, in
turn, probably got the virus by eating fruit contaminated with saliva
or other bodily fluids from bats, according to Pourrut.
Once a human is infected, there is no cure for ebolavirus or
marburgvirus infection. After an incubation period of about a week,
victims rapidly develop high fever, diarrhea, vomiting, respiratory
disorders and hemorrhaging. Death can ensue within a few days. About
a quarter of Marburg hemorrhagic fever cases are fatal, whereas case
fatality rates range from 50 to 80 percent with Ebola hemorrhagic
fever in Africa.
Ebolavirus may circulate naturally within at least one other bat
species and spread to members of the Egyptian rousette via contact
with infected saliva left on fruit remnants, Formenty said in an
interview. Also, no link with the Egyptian fruit bat was found with
at least 3 Ebola hemorrhagic fever outbreaks, he said. “We’ve got a
whole lot of clues on the crossword puzzle and we’re just filling the
blanks now,” said Bob Swanepoel, a virologist at South Africa’s
National Institute for Communicable Diseases in Johannesburg, who 1st
sought to unravel the history of Marburg hemorrhagic fever in the
mid-1970s. Scientists will complete the task within a decade, he said.
2009
In the spring of 2009 I asked her the following questions and then reported her answers here in July of 2009.
Q. There are many people worried about the novel H1N1 virus combining with the H5N1 virus. What are your feelings on the issue?
MA. The HPAI A(H5N1) virus is an avian disease - panzootic in poultry and wild birds - and while there have been over 250 human deaths in the last six years from H5N1 infection there is very limited human-to-human transmission of the virus.
But it is worrisome considering it’s:
1. High lethality
2. Worldwide host reservoir
3. And propensity for mutation
We know, for instance, that in Indonesia the virus may be adapting to pigs.
The H5N1 virus isolated from pigs is less harmful to mice than the H5N1 isolated from chickens.
This means that the virus growing in pigs might well be adapting to a new host - which, in turn, suggest that it might eventually adapt to humans as well.
Pigs are seen as a possible intermediate host that can help in that adaptation because the epithelial cells in pigs’ trachea can be infected by both avian and human flu. Where, in the event of co-infection, viral reassortment might occur.
It seems prudent to be concerned.
However, the normal seasonal flu kills over 30,000 per year which is a quantum leap in risk.
As to the novel H1N1 virus now spreading like wildfire around the globe - the issue is different. The new H1N1 virus is more deadly than common seasonal influenza because of its ability to infect cells deep in the lungs where it can cause scarring and pneumonia.
Also it is more virulent. At least in animal models that is, what we see in the human population is a rather low (0.2%) lethality. Time will tell what the final verdict on virulence is.
We know for certain that it does not have the mitochondrial killing prowess of the 1918 flu virus. However it seems to have spread in six weeks as much as the seasonal flu spreads in six months. It is hot.
As to your question of the two mixing and somehow acquiring the lethality of H5N1 and infectiousness of H1N1 - it is of course possible.
Antigenic shift between avian influenza and human influenza is not something unheard of. The “Asian” flu pandemic of 1957 and the “Hong Kong” flu pandemic of 1968 both introduced novel strains.
The H2 that appeared in 1957 and the H3 that appeared in 1968 came from influenza viruses circulating in birds.
So when we consider that the human population has absolutely no immunity against any H5 viruses the red flags go very high indeed.
Will H5N1 reassort with H1N1 or with H3N2, or will it “drift” into another host like pigs and then move to other mammals?
It has failed over the last few years to combine with H3N2 and has yet to find a non-avian host.
When novel H1N1 becomes ubiquitous, as it certainly appears headed, will the increased opportunity for antigenic shift finally create a specific case of reassortment or viral shift that confers a phenotypic change?
I don’t know. No one does, but we can use our experience and make educated calculations as to the possibilities. I would rate the chance of H1 acquiring a polybasic cleavage site at nil, but the odds of H1 picking up lethal genes or polymorphisms at >5%.
_________________________________________________
This second interview is shorter and a bit less technical the URL is here:
http://www.flutrackers.com/forum/showthread.php?s=e1d8dbc4da841cb9d6b1dd32e6bce470&t=128997