Ebola

Raudfjorden Beach, Svalbard, Norway

The Ebola outbreak has proven to a challenge for worldwide heatlh leaders.  The CDC has information about Ebola on its website, as does the World Health Organization (WHO).  The CDC information is delineated into a number of topical areas of interest to subject audiences.  I'm interested in the etiology of Ebola, its transmission, and issues surrounding its current outbreak.

My interest in Ebola began during my actuarial career, reading the "Hot Zone" , a 1994 non-fiction book about incidents involving viral hemorrhagic fevers, including ebolaviruses and marbug viruses. The memory of the book stayed with me since I was reading it while sailing down the west coast of Vancouver Island in 15 foot swells in a sailing vessel.  I can recall eating copious amounts of ginger cookies to ward off seasickness as I read of hemorrhagic fevers killing off people very quickly, in a very bloody and gory fashion, as all the while I was lurching back and forth in the sea and swell on the Pacific Ocean.  The ginger cookies did their job and the memory is etched in my experience, gone but not forgotten, as Ebola emerges again, this time, expressed  in the news of an outbreak.

These hemorrhagic diseases killed off people before they had a chance to spread extensively, and, were confined to certain areas in Africa and mostly away from major population centers.

According to the CDC, the virus can be spread through direct contact with blood and body fluids of a person infected with Ebola, with objects such as syringes infected with Ebola and infected fruit bats or primates.  The question remains as to factors impacting the geographical distribution of Ebola, how it independently arises, factors of etiology and its potential spread elsewhere.

The recent upswing in the Ebola virus prompted me to question its etiology, transmission and other issues.  For example, because of the increase in number of cases, I wondered if the virus had recombined with another virus to increase its transmission and decrease its mortality, or if there were other factors.   In this blog article I consider a number of issues, and raise some questions relating to the virus.


Etiology

• Does Ebola predate the AIDs/SIV/HIV viruses and does it provide some idea of the origin of these viruses? The CDC expresses that it does not know the origin of the original host of the Ebola Virus;  It is interesting to study the context of the Ebola virus regarding its emergence out of the Kinshasha Highway  across the Congo into Uganda as discussed in "The Hot Zone".  Did the virus have origins in bat habitats such as caves, rock, lava tubes, environments exposed to varying bacteria and archaea?
• The Ebola virus is a negative sense RNA virus. The production of proteins from a negative sense RNA virus require first the production of Messenger RNA (mRNA) and then proteins from mRNA. Ebola does not have reverse transcriptase, which would ordinarily be needed to enable insertion of its genetic contents into the DNA.   Is its 'purpose' then to directly produce mRNA (messenger RNA), and why? Research has shown that the filoviruses behind Ebola are very old and that there is direct insertion of genetic content with indications of evolutionary divergence a long time ago.  - The Lin Edwards article, "Ebola and Marburg viruses may be much older than thought" discusses this subject.
• Does the Ebola virus relate to issues concerning New World Monkeys and Old World Monkeys and the divergence of the two species?  If so, would this tend to indicate the same type of environmental conditions that may have existed at the time of that divergence?
• What is the distribution of the virus?  Does the virus act with regards to specific populations, affecting certain populations in a negative or positive way, and leaving others untouched.  What factors in these populations would account for the outbreak?  Are other populations at risk?

Transmission

• Did the Ebola virus recombine with another virus (for example the Corona Mers Virus  , Seasonal Flu Virus or enteroviruses) to allow it to decrease its mortality rate and increase its transmission?  Is it continuing to do so and would further recombination with the current seasonal flu change it further along these lines? 
• A subject of interest to is transmission of Ebola from the natural host to a target population.  Is Ebola being expressed, sustained within the target population or being sequestered?  Does this imply sequestration in a host for transmission or expression later under circumstances that may enable it to be used as a regulatory operator or a mediator of group identity or expression of  immunity systems?  Is it developing a symbiotic relationship with the host or another virus in a toxin/anti-toxin sort of manner (discussed by my blog article on Dr Luis Villarreal and his work on group identity systems)? How does this concept explain the existence of this virus in a reservoir species?
• What is the risk for the spread of Ebola?  To what extent is the risk environmental and to what extent can it be transmitted from person to person? 
• Is Ebola being transmitted in a less than lethal form under our eyes without our knowledge?
• Can Ebola be spread by more species of animals than listed under the CDC website?  
• How might Ebola change to become more transmissible to a greater variety of populations impacted by different environmental factors?  How would this risk change if the Ebola virus were to combine with the seasonal flu in a variety of different ways?

Geological Factors

• What factors in Africa are most significant in the etiology of Ebola?  Heat, humidity, coeexistence with and diversity of animal species, alkaline environments, carbon dioxide sequestration and outgassing (e.g. Lake Nyos), the Archaean basement substrate of the West African bedrock, granite, uranium, endospores such as bacillus anthracis, and  natural nuclear fission reactors from underground uranium (Gabon)? 
• What is the impact of the African mining fields?  Iron, gold, lead, silver, arsenic, mercury , uranium and nickel are among products of mining.  Nickel has a positive feedback impact on inflammatory markers. 
• How do endospores such as bacillus anthracis  fit into the story of Ebola, set in the mining context of West Africa, with its iron, gold, silver, arsenic, uranium, nickel and mercury, and the expression of inflammatory markers and feedback indicators?
• Are these various environmental issues constrained to Africa or are they present in other environments, and where do other similar environmental conditions exist?  Do these conditions have to exist in the same place or can an individual experience them by exposure to a variety of locations? For example, Archaean basement layers of rock exist in the Arctic, in Svalbard, which I visited in 2005. How would exposure to Archaea and other factors present in West Africa differ from the situation in Svalbard where it is much colder! Where else can we find archaea and chiral substances?
• How do increases in solar radiation  and changes in the Earth's magnetic field impact the expression of Ebola in Africa? To what extent would these factors affect the expression of Ebola in other areas of the planet?

Environment and Physiology

•  Does the emergence of a disease that promotes bleeding have significance as it relates to climate change or other planetary or environmental factors?    Is some environmental change occurring that would result in blood clotting more easily, something that would need to be countered by less viscous blood and changes in the coagulation cascade?
• How might the environmental factors in Africa affect blood coagulation?  Through mitochondrial regulation as it is impacted by environment, haplogroups and uncoupling in oxidative phosphorylation?  Through the impacts of oxygen reactive species?  Through solar radiation, geomagnetic storms and cycles?  Through the Warburg effect  (which replaces aerobic respiration with glycolysis)? Through arsenic mining?  Through positive feedback mechanisms involving hypoxemia  and inflammatory responses?  
• Is it possible that the Archaean basement layer of rock in West Africa impacts the blood coagulation cascade  and the blood vasculature through chirality?  Would concepts of fractal dimension  and tortuosity explain concepts of blood coagulation and vascular inflammation and other disorders, including stroke and cancers, including those of the blood and lymphatic systems?  
• What impact does the water people drink (and breathe through water vapor) impact people, including the impact on group identity systems and physiological parameters?
• Does the outgassing  of carbon dioxide  as a result of global warming, the release of iron from iron sequestered in the rock, and the release of endospores from sequestration, explain any of the natural events happening today, as regards vascular and coagulation issues?
• Is it possible that Ebola, as a disorder that promotes bleeding, developed as a feedback mechanism to counter the impact of increased blood coagulation due to the environmental impacts raised above? 
•  Bleeding may increase as blood coagulation factors are used up; does Ebola act to promote such bleeding to counter increases in clotting factors secondary to these environmental issues?  Is it possible that Ebola thus impacts the regulatory mechanisms of the coagulation cascade?

Detection

• Could an easy detection test be done for Ebola using, for example, saliva? This might prove less expensive and easier to measure for initial testing prior to full blood workups if it was sufficiently sensitive and specific.
• Could the d-dimer test and PPT tests be used as early indicators of Ebola.
• Can a series of early indicators, including markers of respiratory and coagulation system function and exposure to certain environmental factors, be developed to ascertain risk patterns for specific populations?  
• Where might the solution to Ebola be found?  Only time will tell.  Are lamprey VLR's a potential solution for isolating, detecting, and finding a cure for Ebola, considering their ability to detect bacillus anthracis and their affinity for carbohydrate glycoproteins?  Considering the age of the filoviruses and the characteristics of Ebola itself, is this a potential area to investigate?

Summary

Does the emergence of Ebola reflect the re-emergence of ancient historical patterns?  Have these patterns been carried by reservoir species from the depths of time to the particular victims of Ebola? Will Ebola adapt and spread elsewhere or re-emerge in other parts of the planet, independently?

Are the issues happening in West Africa an early indicator ('Canary in a Coal Mine')  of planetary changes?  These changes include changes in Earth's magnetic field, climate change, global warming and solar radiation, and downstream effects including release of sequestered minerals and gases such as carbon dioxide and methane from rock and oceans.  These are all areas of concern.  Historical examples of changes in Earth's magnetic field are shown over longer periods of time and more recent geologic time periods in this Wikipedia article on the Earth's Magnetic Field.

Finally, I am reminded of the childhood game, "Animal, vegetable or mineral" and associations with the "Tree of Life" (and probably, by extension, "The Tree of Good and Evil").  Ebola is a disease with a past, reflecting deep phylogeny and the rivers of time as embedded in the history of our rocks.

Sources:

marilyndunstan.blogspot.com
Evolution of Adaptive Immunity

Wikipedia:
Ebola virus disease
"The Hot Zone"
Kinshasha Highway
Archaea
Sense (molecular biology)
Messenger RNA
Reverse Transcriptase
Filoviridae
New World Monkey
Lake Nyos
Endospore
Bacillus Anthracis
Natural nuclear fission reactor
Nickel
Chirality
Sunlight
Earth's Magnetic Field
Oxidative Phosphorylation
Reactive Oxygen Species
Geomagnetic Storm
Warburg Effect
Glycolysis
Coagulation Cascade
Fractal Dimension
Tortuosity
Outgassing
Carbon Sequestion
Animal Sentinel
Earth's Magnetic Field-Geomagnetic Polarity
Earth's Magnetic Field-Brunhes Geomagnetism
Earth's Magnetic Field

World Health Organization:
Ebola Virus Disease

CDC:
CDC
Ebola (Ebola Virus Disease
2014 Ebola Outbreak in West Africa (Outbreak Distribution Map)

Phys Org: 
Ebola and Marburg Viruses May be Much Older Than Thought

JoVE Visualize: Anthrax lethal toxin inhibits translation of hypoxia inducible factor 1? and causes decreased tolerance to hypoxic stress

Geology and Mineral Resources of West Africa - The Archaean Basement

National Academy of Sciences: High-affinity lamprey VLRA and VLRB monoclonal antibodies

Berkeley Lab: Structure of the Ebola Virus Glycoprotein Bound to an Antibody from a Human Survivor

NASA Science News - Earth's Inconsistent Magnetic Field

Mt St Helens and other Cascade Volcanoes

Mt St Helens Crater shrouded by clouds, May 16, 2011 (Image on Photoshelter)

In a recent blog article on Mt St Helen’s 31st anniversary, I discussed a visit to the Mt St Helens National Volcanic Monument and displayed some images of earlier 2006 volcanic steam activity.

Today, in 2011, Mt St Helens today is relatively peaceful. The U.S.G.S. Cascade Volcano Observatory has assigned it a “normal” rating (since July 2008) reflecting its relative quiet. The explosive eruption (and buildup) of May 18, 1980 is far behind us, and the volcano has left some distance between the eruptions of 2004-8 and today. The image shows clouds dancing across the crater, not steam of volcanic origin.

Indications are that Mt St Helens will continue its eruptive activity and is likely to erupt again in this century. (Mt St Helens - A 30 Year Legacy of Volcansim - EOS-AGU). This is based on its age and past history.

In my last article, “Calculating Odds and Probabilities” I discussed the assessment of various odds and probabilities ranging from coin tosses to weather forecasting. It is clear that some predictions are relatively straightforward and others are incredibly complex.

The events, risks and probabilities associated with volcanic hazards present a great challenge because of the wide ranging risks, the variability of impacts and the low probabilities of occurrence associated with very high impact events.

Mt St Helens showed us in 1980 that a low probability, high impact event can happen in our lifetime and region (Washington State). While Mt St Helens is the most active of Cascade Volcanoes, the other Cascade Volcanoes are also of interest.


The USGS provides an interactive map of the Cascade Volcanoes from Washington to Northern California. The summary provides a broad overview picturing the scope of Cascade Volcanoes throughout the region. The map/page provides links to each of the Cascade Volcano “Visit a Volcano Site” providing a photo and information for each volcano.

The difficulty in assessing the risk associated with an event, whether it is meteorological or seismic, is in assessing the probability that it will occur, the severity of the event should it occur, and the impact on the population.

The USGS has done a great deal of work in identifying hazards for the Cascade volcanoes. The Mount St Helens eruption, and other volcanic eruptions have allowed geologists to gain a great deal of information regarding volcanic hazards, and develop advanced monitoring technologies to allow them to better manage volcanic risk.

A USGS Fact Sheet (What are Volcano Hazards?) describes Volcano hazards, both in text and with a graphic that displays the hazards on a simplified Cascade volcano.

The hazards shown in the Fact Sheet include hazards that we saw with the 1980 Mt St Helens eruption. The pyroclastic flow that blasted down numerous trees, scorched others and killed people. The towering ash cloud that rained ash fall on Eastern Washington and continued around the world. The debris flows that sculptured the landscape in destructive lahars , racing down the Toutle River, washing out bridges and silting up the Columbia River.

Entrance to Ape Cave, Mt St Helens National Volcanic Monument (Image on Flickr)

In addition, we see the impact of much earlier lava flows in Mt St Helen’s Ape Cave Lava Tube. Ape Cave contains the continental United States’ longest continuous lava tube, occurring around 2,000 years ago in the Cave Basalt.

Cascade volcanoes have an extensive volcanic history, as displayed in a display of their eruptive history over the past 4,000 years which is available as a pdf or poster to order from USGS.

We can look at the chart of volcanic history and wonder given the frequency and time since last eruption, whether a particular mountain is “due” for an eruption. We do know that future eruptions may occur, we simply may not know when. Once volcanic activity has started, geologists are better able to monitor and respond to the ongoing situation.

It is a matter of living with uncertainty and managing risks.

The USGS has comprehensive risk assessments for each Cascade Volcano. More information can be obtained through the USGS’s Cascade Volcano Observatory Website.

Mt St Helens 31st Anniversary of May 18, 1980 Eruption

Aerial View of Steam Eruption, Mt St Helens, May 20, 2006, taken from Johnston Ridge Observatory, Mt St Helens National Volcanic Monument, Washington (image on Photoshelter)

Thirty-one years ago, at 8:32 am on May 18, 1980, Mt St Helens erupted, in a cataclysmic eruption, that would change the face of the environment and sow the seeds of future renewal. Nature has its way of promoting renewal, through cycles of creation and destruction, and nowhere is this more evident than at Mt St Helens, where the volcano and environs continue to emerge in their new environment shaped by the vehicles of geological change.

Mt. St Helens National Monument can be reach from I-5 southbound at Toledo, SR 505, or from I-5 northbound at Castle Rock, SR 504 (Spirit Lake Highway). I took the latter route, visiting Washington State’s Silver Lake Visitor Center, 5 miles east along SR 504, and took in their presentation on the Mt St Helens Eruption “Cycle of Chaos and Creation”.

I entered Mt St Helens National Volcanic Monument, stopping at Hoffstadter Bluffs Visitor Center, enjoying a view of Mt St Helens in the distance and an excellent Elk Burger in their dining area before heading up to Johnston Ridge Observatory. As you drive towards Johnston Ridge Observatory, there are opportunities to pull over and enjoy differing views of the mountain as you get closer, including at the Elk Rock and Loowit Viewpoints.

The sense of closeness to the volcano becomes more than distance as you become more and more aware of the impact of the blast area on the landscape. Even as it is being transformed, being renewed, you are aware that there are thirty-one years of renewal, and that contrasts with the age of the landscape you left behind.





Mt St Helens Steam Eruption, May 20, 2006, viewed from Hummocks Trail showing renewal of vegetation, Mt St Helens National Volcanic Monument (image on Photoshelter)

The road heads downward before the last ascent to the Johnston Ridge Observatory. The Hummocks Trail provides an opportunity to hike amongst the hummocks, created by the Mt St Helens debris avalanche. The debris avalanche created by the eruption of Mt St Helens offered geologists an opportunity to learn about and identify such formations elsewhere.

From the Hummocks Trail, the road then climbs upwards towards Johnston Ridge Observatory at 4,255 feet. As you hike up an incline from the parking lot towards the Visitor Center, you are greeted with a marvelous view of Mt St Helens, looking right down into the throat of the volcano. It is up close and personal, looming as a reminder of the blast impact, as the crater opens up its giant maw to the visitor, you are struck by the awesome power that so forcefully reconstructed the landscape in the wake of its eruption.

As the clouds dance across the crater and the lava dome inside it, you are reminded that Mt St Helens, the youngest of Cascade volcanoes, has not been quiet since it’s May 18, 1980 eruption. Eruptive activity continued into 1986 and then resumed during 2004-2006, including dome building activity.

A visit to the Visitor Center gives the opportunity to explore exhibits, view a movie, “Message from the Mountain”, and attend ranger-guided talks. In one talk, the ranger used still photographs to illustrate various stages of Mt St Helens’s activity leading up to and including the eruption events. We saw Mt St Helens’s pre-eruptive recreational splendor as a near-perfect volcanic cone and glimpses of pre-eruptive awakenings.

As explained by the ranger, volcanic activity beneath the surface of the volcano eroded and weakened the rock structure on the side of the mountain, turning it to clay. This weakened area provided an opportunistic path for the upwelling magma to take, versus the hardened rock plug at the top of the volcano. The side of the mountain bulged with pressure and structural weakening. The landslide and accompanying 5.1 earthquake triggered the event that would unleash the power and fury of Mt St Helens, with resultant lateral blast, pyroclastic flows, lahars (mud flows) and an ejection of ash that would circle the globe.

It is sobering to realize that volcanism can eat away at a mountain’s rock structure from within, weakening it and exposing the mountain to risk of collapse. It is yet another example of a “tipping point” where a marginal change can have a result out of proportion to its own magnitude.

Geologists and volcanologists study volcanoes and other geological system and we are all continually learning from their experience. Johnston Ridge Observatory was named in memory of geologist David Johnston, volcanologist, who witnessed the May 18, 1980 eruption from what is now Johnston Ridge, and radioed in the message “Vancouver, Vancouver, this is it” before perishing in the blast.

The Mt St Helens 1980 eruption has resulted in a continued expansion in knowledge and monitoring tools for understanding the behavior of volcanoes.

In one study, the impacts of volcanic hydrothermal systems on Cascade volcanoes is being studied by the United States Geological Survey.

A wide range of information about Cascade Volcanoes can be found on the Cascade Volcano Observatory (CVO) site.