Nika
Well-known member
For officially released info from the Dallas Ebola site
Link to the Dallas Ebola EOC
http://www.dallascityhall.com/updates/index.html
Link to the Dallas Ebola EOC
http://www.dallascityhall.com/updates/index.html
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Dallas TX Ebola Emergency Operations Center
- Thread starter Nika
- Start date
AlaskaDenise
In Memoriam
Re: Dallas TX Ebola Emergency Operations Center
The FACT SHEET is very informative.
They point out that transmission can occur from surfaces contaminated by a person's body fluids - not just pure direct contact.
They mention that recover depends on the person's immune response, and that antibodies last for 10 years!
.
The FACT SHEET is very informative.
They point out that transmission can occur from surfaces contaminated by a person's body fluids - not just pure direct contact.
They mention that recover depends on the person's immune response, and that antibodies last for 10 years!
.
Re: Dallas TX Ebola Emergency Operations Center
Hi Denise. It's been a while.
Keep in mind that there are at least 5 known variations of ebola and my understanding is being infected with one variation does not confer immunity to the others.
http://www.sciencedaily.com/releases/2014/09/140909123603.htm
Due to unknown reasons, there are also substantial numbers of people in west africa who are immune:
http://www.nytimes.com/2014/09/06/health/ebola-immunity.html
Hi Denise. It's been a while.
Keep in mind that there are at least 5 known variations of ebola and my understanding is being infected with one variation does not confer immunity to the others.
http://www.sciencedaily.com/releases/2014/09/140909123603.htm
Due to unknown reasons, there are also substantial numbers of people in west africa who are immune:
http://www.nytimes.com/2014/09/06/health/ebola-immunity.html
AlaskaDenise
In Memoriam
Re: Dallas TX Ebola Emergency Operations Center
Hi again Zac!
Topics covered in that article (superior immune system, natural immunity, etc.) remind me about some very old discussions here on FT about "superspreaders" - those who carry a pathogen, yet never get infected. I can't remember all the details, but I think it involved a superior immune system that kept the viral levels low enough to not produce symptoms, yet high enough to pass virons on to others. I believe something like that also happens with a small percentage of HIV infections. Then there's the ultimate-survivors theory - where many species have about 5% of their population that is resistant to most all pathogens - so in the event of a major plague, there will always be a remnant population that can restart propagating the population.
Some of these ideas MAY be happening with ebola.
.
Hi again Zac!
Topics covered in that article (superior immune system, natural immunity, etc.) remind me about some very old discussions here on FT about "superspreaders" - those who carry a pathogen, yet never get infected. I can't remember all the details, but I think it involved a superior immune system that kept the viral levels low enough to not produce symptoms, yet high enough to pass virons on to others. I believe something like that also happens with a small percentage of HIV infections. Then there's the ultimate-survivors theory - where many species have about 5% of their population that is resistant to most all pathogens - so in the event of a major plague, there will always be a remnant population that can restart propagating the population.
Some of these ideas MAY be happening with ebola.
.
Nika
Well-known member
Re: Dallas TX Ebola Emergency Operations Center
Ebola Marburg and other nasty hemorrhagic fevers have been shown to stably integrate into vertebrate genomes and potentially confer some protective advantage.
Its a deeply fascinating subject and if i were to go back to school for a second PhD i would do it on viral mediated molecular evolution.
Here is a nice paper on this topic
Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes
Vladimir A. Belyi, Arnold J. Levine, Anna Marie Skalka
Vertebrate genomes contain numerous copies of retroviral sequences, acquired over the course of evolution. Until recently they were thought to be the only type of RNA viruses to be so represented, because integration of a DNA copy of their genome is required for their replication. In this study, an extensive sequence comparison was conducted in which 5,666 viral genes from all known non-retroviral families with single-stranded RNA genomes were matched against the germline genomes of 48 vertebrate species, to determine if such viruses could also contribute to the vertebrate genetic heritage. In 19 of the tested vertebrate species, we discovered as many as 80 high-confidence examples of genomic DNA sequences that appear to be derived, as long ago as 40 million years, from ancestral members of 4 currently circulating virus families with single strand RNA genomes. Surprisingly, almost all of the sequences are related to only two families in the Order Mononegavirales: the Bornaviruses and the Filoviruses, which cause lethal neurological disease and hemorrhagic fevers, respectively. Based on signature landmarks some, and perhaps all, of the endogenous virus-like DNA sequences appear to be LINE element-facilitated integrations derived from viral mRNAs. The integrations represent genes that encode viral nucleocapsid, RNA-dependent-RNA-polymerase, matrix and, possibly, glycoproteins. Integrations are generally limited to one or very few copies of a related viral gene per species, suggesting that once the initial germline integration was obtained (or selected), later integrations failed or provided little advantage to the host. The conservation of relatively long open reading frames for several of the endogenous sequences, the virus-like protein regions represented, and a potential correlation between their presence and a species' resistance to the diseases caused by these pathogens, are consistent with the notion that their products provide some important biological advantage to the species. In addition, the viruses could also benefit, as some resistant species (e.g. bats) may serve as natural reservoirs for their persistence and transmission. Given the stringent limitations imposed in this informatics search, the examples described here should be considered a low estimate of the number of such integration events that have persisted over evolutionary time scales. Clearly, the sources of genetic information in vertebrate genomes are much more diverse than previously suspected.
Author Summary
Vertebrate genomes contain numerous copies of retroviral sequences, acquired over the course of evolution. Until recently they were thought to be the only type of RNA viruses to be so represented. In this comprehensive study, we compared sequences representing all known non-retroviruses containing single stranded RNA genomes, with the genomes, , with the genomes of 48 vertebrate species. We discovered that as long ago as 40 million years, almost half of these species acquired sequences related to the genes of certain of these RNA viruses. Surprisingly, almost all of the nearly 80 integrations identified are related to only two viral families, the Ebola/ Marburgviruses, and Bornaviruses, which are deadly pathogens that cause lethal hemorrhagic fevers and neurological disease, respectively. The conservation and expression of some of these endogenous sequences, and a potential correlation between their presence and a species' resistance to the diseases caused by the related viruses, suggest that they may afford an important selective advantage in these vertebrate populations. The related viruses could also benefit, as some resistant species may provide natural reservoirs for their persistence and transmission. This first comprehensive study of its kind demonstrates that the sources of genetic inheritance in vertebrate genomes are considerably more diverse than previously appreciated.
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001030
Citation: Belyi VA, Levine AJ, Skalka AM (2010) Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes. PLoS Pathog 6(7): e1001030. doi:10.1371/journal.ppat.10010
Ebola Marburg and other nasty hemorrhagic fevers have been shown to stably integrate into vertebrate genomes and potentially confer some protective advantage.
Its a deeply fascinating subject and if i were to go back to school for a second PhD i would do it on viral mediated molecular evolution.
Here is a nice paper on this topic
Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes
Vladimir A. Belyi, Arnold J. Levine, Anna Marie Skalka
Vertebrate genomes contain numerous copies of retroviral sequences, acquired over the course of evolution. Until recently they were thought to be the only type of RNA viruses to be so represented, because integration of a DNA copy of their genome is required for their replication. In this study, an extensive sequence comparison was conducted in which 5,666 viral genes from all known non-retroviral families with single-stranded RNA genomes were matched against the germline genomes of 48 vertebrate species, to determine if such viruses could also contribute to the vertebrate genetic heritage. In 19 of the tested vertebrate species, we discovered as many as 80 high-confidence examples of genomic DNA sequences that appear to be derived, as long ago as 40 million years, from ancestral members of 4 currently circulating virus families with single strand RNA genomes. Surprisingly, almost all of the sequences are related to only two families in the Order Mononegavirales: the Bornaviruses and the Filoviruses, which cause lethal neurological disease and hemorrhagic fevers, respectively. Based on signature landmarks some, and perhaps all, of the endogenous virus-like DNA sequences appear to be LINE element-facilitated integrations derived from viral mRNAs. The integrations represent genes that encode viral nucleocapsid, RNA-dependent-RNA-polymerase, matrix and, possibly, glycoproteins. Integrations are generally limited to one or very few copies of a related viral gene per species, suggesting that once the initial germline integration was obtained (or selected), later integrations failed or provided little advantage to the host. The conservation of relatively long open reading frames for several of the endogenous sequences, the virus-like protein regions represented, and a potential correlation between their presence and a species' resistance to the diseases caused by these pathogens, are consistent with the notion that their products provide some important biological advantage to the species. In addition, the viruses could also benefit, as some resistant species (e.g. bats) may serve as natural reservoirs for their persistence and transmission. Given the stringent limitations imposed in this informatics search, the examples described here should be considered a low estimate of the number of such integration events that have persisted over evolutionary time scales. Clearly, the sources of genetic information in vertebrate genomes are much more diverse than previously suspected.
Author Summary
Vertebrate genomes contain numerous copies of retroviral sequences, acquired over the course of evolution. Until recently they were thought to be the only type of RNA viruses to be so represented. In this comprehensive study, we compared sequences representing all known non-retroviruses containing single stranded RNA genomes, with the genomes, , with the genomes of 48 vertebrate species. We discovered that as long ago as 40 million years, almost half of these species acquired sequences related to the genes of certain of these RNA viruses. Surprisingly, almost all of the nearly 80 integrations identified are related to only two viral families, the Ebola/ Marburgviruses, and Bornaviruses, which are deadly pathogens that cause lethal hemorrhagic fevers and neurological disease, respectively. The conservation and expression of some of these endogenous sequences, and a potential correlation between their presence and a species' resistance to the diseases caused by the related viruses, suggest that they may afford an important selective advantage in these vertebrate populations. The related viruses could also benefit, as some resistant species may provide natural reservoirs for their persistence and transmission. This first comprehensive study of its kind demonstrates that the sources of genetic inheritance in vertebrate genomes are considerably more diverse than previously appreciated.
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1001030
Citation: Belyi VA, Levine AJ, Skalka AM (2010) Unexpected Inheritance: Multiple Integrations of Ancient Bornavirus and Ebolavirus/Marburgvirus Sequences in Vertebrate Genomes. PLoS Pathog 6(7): e1001030. doi:10.1371/journal.ppat.10010
Re: Dallas TX Ebola Emergency Operations Center
As of 2 weeks ago, the head of the NIH virology lab said that their diagnostic tests were based on the Sierra Leone virus. That suggests only the virus strains from the Sierra Leone cases had been sequenced. It appears from his statement that there were multiple strains of the virus in circulation. And some of the cases did not match the DNA sequence(s) they had selected for detecting the virus.
From a recent Q&A with a NIH research who was in africa:
Q: Is there any genetic data from Ebola strains in Liberia?
A: Right now our diagnostics is largely based on sequence data from Sierra Leone. But it has become very, very important to get the sequence of the currently circulating virus strains in Liberia to make sure that our assays are working properly. There is one gene target that we are not using anymore because we were missing cases.
Q: At the moment, you are storing some blood samples from patients in Monrovia, but you’re not sending any samples out to be sequenced?
A: No, and that is a very common situation. It goes into the discussion of intellectual property. In my view the owner of the specimen is the patient, first of all, and then the country, so the ministry of health or the government. So in order to bring samples out of Liberia there needs to be some kind of agreement in place that this is allowed, and that takes time. People are working on a memorandum of understanding and I think and hope we're going to get it very quickly. But you cannot just export clinical samples without proper permission.
http://news.sciencemag.org/africa/2014/09/confronting-ebola-virologist-liberias-hot-zone
As of 2 weeks ago, the head of the NIH virology lab said that their diagnostic tests were based on the Sierra Leone virus. That suggests only the virus strains from the Sierra Leone cases had been sequenced. It appears from his statement that there were multiple strains of the virus in circulation. And some of the cases did not match the DNA sequence(s) they had selected for detecting the virus.
From a recent Q&A with a NIH research who was in africa:
Q: Is there any genetic data from Ebola strains in Liberia?
A: Right now our diagnostics is largely based on sequence data from Sierra Leone. But it has become very, very important to get the sequence of the currently circulating virus strains in Liberia to make sure that our assays are working properly. There is one gene target that we are not using anymore because we were missing cases.
Q: At the moment, you are storing some blood samples from patients in Monrovia, but you’re not sending any samples out to be sequenced?
A: No, and that is a very common situation. It goes into the discussion of intellectual property. In my view the owner of the specimen is the patient, first of all, and then the country, so the ministry of health or the government. So in order to bring samples out of Liberia there needs to be some kind of agreement in place that this is allowed, and that takes time. People are working on a memorandum of understanding and I think and hope we're going to get it very quickly. But you cannot just export clinical samples without proper permission.
http://news.sciencemag.org/africa/2014/09/confronting-ebola-virologist-liberias-hot-zone
AlaskaDenise
In Memoriam
Re: Dallas TX Ebola Emergency Operations Center
Some admitting forms include the provision that the facility can use samples from your body!
.
Some admitting forms include the provision that the facility can use samples from your body!
.
AlaskaDenise
In Memoriam
Re: Dallas TX Ebola Emergency Operations Center
Nika: That paper reminds me of something I read about an ancient retrovirus that became part of the human/guinea pig/fruit bat/??? DNA and silenced the part of mammalian DNA that normally converts blood glucose into ascorbate - hence the support for high serum levels of vitamin C.
What I'm really curious about here is whether some people aren't getting ebola because of something peculiar to their immune system, without the necessity of ebola antibodies. In links I posted elsewhere, the 2 anticancer drugs work partially by reducing viral replication, but they're not sure how. The SERMs that are normally used for their ER antagonist properties, also manipulate metabolic processes, etc. so they don't know exactly how they exert an influence on ebola because there wasn't a motive for researching that pathway.
.
Nika: That paper reminds me of something I read about an ancient retrovirus that became part of the human/guinea pig/fruit bat/??? DNA and silenced the part of mammalian DNA that normally converts blood glucose into ascorbate - hence the support for high serum levels of vitamin C.
What I'm really curious about here is whether some people aren't getting ebola because of something peculiar to their immune system, without the necessity of ebola antibodies. In links I posted elsewhere, the 2 anticancer drugs work partially by reducing viral replication, but they're not sure how. The SERMs that are normally used for their ER antagonist properties, also manipulate metabolic processes, etc. so they don't know exactly how they exert an influence on ebola because there wasn't a motive for researching that pathway.
.
Nika
Well-known member
Re: Dallas TX Ebola Emergency Operations Center
Am super woozy from sleep but will revisit this in the AM. On the most recent TWIV they mention something about metabolic interplay between mitohondria peroxisomes their ratios and viral lifecycle. If i can dig that up right quick i will if not, tomorrow.
Am super woozy from sleep but will revisit this in the AM. On the most recent TWIV they mention something about metabolic interplay between mitohondria peroxisomes their ratios and viral lifecycle. If i can dig that up right quick i will if not, tomorrow.
Nika
Well-known member
Re: Dallas TX Ebola Emergency Operations Center
http://www.twiv.tv/twiv-304-letters/
Taken from that link:
"On the most recent TWiV (#303 – Borna this way), while discussing the quirks of bats in relationship to viral infections (~00:25:30), Vincent brought up the duplications of genes involved in oxidative stress due to the higher metabolism, which got me thinking about a paper my graduate lab recently published about the relationship between mitochondria, peroxisomes, and anti-viral signaling ( http://kaganlab.com/pdfs/2014_Odendall et al.pdf )
The lab had previously shown that the cytosolic RNA sensors (RIG-I like receptors) can engage their signaling pathway from two locations: mitochondria or peroxisomes. The take home-from this new paper is that the signaling pathways engaged are different – signaling from mitochondria induces type-I interferons, while signaling from peroxisomes induces production of type-III interferons.
Not much is known about the difference between type-I and type-III interferons since until now, everyone had observed them as co-regulated (and the dominant type-III isn’t expressed in mice), but one interesting thing this paper showed is that as cells get more peroxisomes relative to mitochondria, they increase type-III interferon production, and if you eliminate mitochondria from cells entirely, you get a dramatic increase.
Back to the bats: their altered metabolism almost certainly affects their mitochondria/peroxisome ratio, and this could lead to dramatic differences in their antiviral responses. This could also explain why they’re more tolerant to a lot of viral infections that we’re not – does anyone know if this is more often the case with RNA than with DNA viruses?"
http://www.twiv.tv/twiv-304-letters/
Taken from that link:
"On the most recent TWiV (#303 – Borna this way), while discussing the quirks of bats in relationship to viral infections (~00:25:30), Vincent brought up the duplications of genes involved in oxidative stress due to the higher metabolism, which got me thinking about a paper my graduate lab recently published about the relationship between mitochondria, peroxisomes, and anti-viral signaling ( http://kaganlab.com/pdfs/2014_Odendall et al.pdf )
The lab had previously shown that the cytosolic RNA sensors (RIG-I like receptors) can engage their signaling pathway from two locations: mitochondria or peroxisomes. The take home-from this new paper is that the signaling pathways engaged are different – signaling from mitochondria induces type-I interferons, while signaling from peroxisomes induces production of type-III interferons.
Not much is known about the difference between type-I and type-III interferons since until now, everyone had observed them as co-regulated (and the dominant type-III isn’t expressed in mice), but one interesting thing this paper showed is that as cells get more peroxisomes relative to mitochondria, they increase type-III interferon production, and if you eliminate mitochondria from cells entirely, you get a dramatic increase.
Back to the bats: their altered metabolism almost certainly affects their mitochondria/peroxisome ratio, and this could lead to dramatic differences in their antiviral responses. This could also explain why they’re more tolerant to a lot of viral infections that we’re not – does anyone know if this is more often the case with RNA than with DNA viruses?"