first discovered in 1976.
Ebola Why am I fighting to live if I'm just living to fight?
Why am I trying to see when there ain't nothing in sight?
Why am I trying to give when no one gives me a try?
Why am I dying to live if I'm just living to die?
So I'll keep fighting to live till there's no reason to fight
And I'll keep trying to see until the end is in sight
You know I'm trying to give so c'mon give me a try
You know I'm dying to live until I'm ready to die
"DYING TO LIVE" - BIGGIE, TUPAC & EMINEM (FT. EDGAR WINTER)
| Hemispherx Biopharma, Inc. |
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| Ibio, Inc. |
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| NanoViricides, Inc. |
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| Biocryst Pharmaceuticals, Inc. (MM) |
| Inovio Pharmaceuticals, Inc. |
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| Newlink Genetics Corp. (MM) |
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| Sarepta Therapeutics, Inc. (MM) |
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| Tekmira Pharmaceuticals Corp (MM) |
| Glaxosmithkline |
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Vaccine Development, Testing, and Regulation
Vaccine development is a long, complex process, often lasting 10-15 years and involving a combination of public and private involvement.
The current system for developing, testing, and regulating vaccines developed during the 20th century as the groups involved standardized their procedures and regulations. 9/30 First US Case of EBOLAv Reported In Dallas,TX
Soldiers have been deployed to the streets of Liberia to prevent panic as fears spread about the deadly virus.
Troops deploy in Sierra Leone, Liberia to try to prevent the spread of panic about the deadly Ebola virus
AUGUST 2, 2014 The Agent
Ebola viruses cause a severe and often deadly illness known as Ebola virus disease (EVD, also referred to as Ebola hemorrhagic fever). Fatality rates during EVD outbreaks can be as high as 90 percent. Ebola viruses produce hemorrhagic fever, a condition that also can be brought about by other types of viruses but Ebola produces one of the most lethal forms. In addition to the other symptoms of hemorrhagic fever – fever, headache, aches, weakness, vomiting, and diarrhea – the more severe cases can include damage to blood vessels and extensive internal and external bleeding (hemorrhage). Mortality rates for EVD range from 50 percent to 90 percent, with death usually occurring as a result of shock rather than blood loss. The virus is transmitted through direct contact with blood or other body fluids of infected persons or animals, including close contact with deceased Ebola-infected patients.
Ebola viruses belong to a family of viruses termed Filoviridae, which are characterized by a long filamentous structure. There are five subtypes of Ebola viruses: Zaire, Sudan, Bundibugyo, Tai Forest (formerly known as Côte d’Ivoire), and Reston, each named after the location in which it was first identified. The first three subtypes have been associated with large EVD outbreaks in Africa. The Reston subtype is found in the Western Pacific and although it is highly pathogenic in nonhuman primates, it is not known to cause illness in humans.
Ebola was first recognized in 1976 as the cause of twin outbreaks of disease near the Ebola River in the Democratic Republic of the Congo (then known as Zaire) and in a region of Sudan. Some 300 people in each country became infected. The mortality rate was 88 percent in Zaire and 53 percent in Sudan (the Zaire subtype is the most deadly). Although the circumstances of the original human infections are not known, the disease spread through close direct contact and as a result of unsafe and unsanitary hospital practices, such as the use of contaminated needles and the lack of sufficient containment measures. Sporadic and smaller outbreaks have erupted over the succeeding years in the Democratic Republic of the Congo, Gabon, Uganda, and Sudan.
The Reston subtype of Ebola virus was first identified in 1989 in the United States in monkeys housed in a quarantine facility in Reston, Virginia. At least four humans became infected, but none became ill. Additional outbreaks of the Reston subtype occurred between 1989 and 1996 in Texas, Pennsylvania, and Italy. No humans suffered illness in any of these cases. The source of all the Reston subtype outbreaks was traced to a single facility in the Philippines that exported the monkeys. In July of 2009, the discovery of the Reston subtype in domestic pigs in the Philippines was reported. Genetic analysis suggests that the virus has been widely circulating in swine for many years, possibly even before the 1989 outbreak in the United States. The virus has been detected in farmers who have had contact with infected pigs, but they have not shown any signs of illness.
Courtesy: CDC Frederick A. Murphy
Where does the Ebola virus go in between outbreaks? As with other viruses, the survival of Ebola depends upon a host organism(s). Humans are not the host organism - or natural reservoir - of Ebola viruses. Humans become infected when they come into contact with an infected host, although once humans become infected they can transmit Ebola to other people. The identification of the natural reservoir of a virus is of great interest to scientists, because this knowledge gives information as to the geographic range and ecological areas where humans may come in contact with animals or insects that may be the source of the disease; this may allow scientists to more readily contain outbreaks. The natural reservoir of Ebola appears to be the fruit bat. Researchers found evidence that three species of captured fruit bats showed evidence of symptomless infection – that is the bats had Ebola-specific genetic sequences in their bodies or evidence of an immune response to Ebola even though they did not exhibit signs of the disease. Fruit bats live in regions of Africa that include areas where Ebola outbreaks have occurred and are eaten by people in central Africa and may play a key role in transmitting Ebola to great apes and humans. Bats have been implicated as a reservoir of other viruses that cause deadly diseases including SARS and Marburg, a virus related to Ebola that also causes hemorrhagic fever.
In the spring of 2014, a large and rapidly spreading outbreak of EVD erupted for the first time in West Africa. The initial cases in Guinea were reported to the World Health Organization in mid-March and soon thereafter cases were reported in Liberia and then Sierra Leone. Multiple regions in these countries are affected. The virus that is causing this outbreak is very closely related to the Zaire Ebola virus. As of July 2014, there have been approximately 1000 cases reported in these three countries, and over 600 deaths.
Ebola virus is a class A bioterrorism agent, known to cause highly lethal hemorrhagic fever. The mortality rate can be as high as 90 percent. Because the Ebola virus is so hazardous, it is classified as a biosafety level 4 agent - the level assigned to the most dangerous agents known. Research using Ebola viruses requires facilities with the utmost levels of containment, strict controls on access, and highly trained personnel.
There is no cure for Ebola virus disease, no established drug therapy to treat Ebola infection, and no vaccine that can protect humans against Ebola. Scientists lack sufficient diagnostic tools to rapidly identify Ebola infections. Scientists also need a more thorough understanding about how the virus is transmitted and how it causes disease.
Ebola is a threat not only to humans but also to our closest living relatives - the great apes. The western lowland gorilla populations have been decimated by Ebola to such an extent that they are now considered "critically endangered". About a third of the gorillas in protected areas have died from Ebola in the past 15 years. Scientists are concerned that their numbers may not be able to recover and fear that they could become extinct in as soon as a decade.
In addition to being classified as a potential bioterrorism agent, the risk of continued natural outbreaks or the further emergence of Ebola is a serious concern. As the human population grows, human contact with bats or Ebola-infected non-human primates increases. The discovery of the Reston subtype of Ebola virus in pigs introduces the additional possibility of transfer of Ebola virus to humans from pigs. Although the Reston subtype has not caused illness in humans to date, it is possible that the virus could become more dangerous after passage through pigs because they are ideal hosts in which viruses can mix and mutate.
As the emergence of Ebola virus in West Africa in 2014 demonstrates, Ebola continues to be a threat to humans. The latest outbreak of EVD has surpassed previous outbreaks to become the most deadly to date, with over 600 deaths and climbing. As of July 2014, it still has not been contained.
The most recent Ebola outbreak is unprecedented for several reasons. First, it has occurred in a region of Africa in which Ebola has never before been detected. Second, it has spread rapidly and to both rural and urban areas. It has crossed borders to involve multiple regions in three different countries. Because it encompasses a much wider geographic area than in previous outbreaks, containment is vastly more difficult.
It is a great challenge to the medical community in this impoverished area of the world to control the outbreak by identifying, quarantining, and providing medical care to infected individuals. Workers also need to educate a fearful population about the dangers of Ebola and the proper procedures needed to minimize further infections. Indeed, the health care workers themselves are at high risk of infection. The continued spread of Ebola within these countries, and beyond, is a serious concern.
One of the key steps in any virus infection occurs very early in an infection cycle. That is the step where a virus binds to and enters a cell in a susceptible host organism. Because viruses are too small to reproduce on their own, they must invade a host cell in order to multiply and produce more copies of themselves that can then go on to infect other organisms and continue the infection cycle.
Many viruses require a specific protein or other type of molecule on the surface of the host cell - called a receptor - which allows the virus to pass into a cell of a host organism. If an organism or cell type does not possess this particular receptor, the virus is unable to infect that organism or cell type. Knowing what this receptor is for any particular virus is a crucial piece of information for scientists, because it tells them which organisms or cell types are susceptible to infection by a certain virus. Furthermore, this knowledge can be used to design therapies that may be able to prevent a virus from entering into a cell and initiating an infection.
Precisely how the Ebola virus enters cells is unknown at present. It is known that in humans, the Ebola virus appears to infect many different cell types. Ebola is also thought to have a broad host range, since it is capable of infecting diverse mammalian species, including primates, rodents, and bats.
Dr. Richard Sutton, while in the Department of Molecular Virology and Microbiology at Baylor College of Medicine, worked to identify the elusive Ebola virus receptor. Based on evidence from other scientists that suggested that members of a group of proteins named the Tyro3 family might mediate entry of Ebola virus into cells, Dr. Sutton’s group tested what would happen if they reduced the levels of the Tyro3 proteins in cells. They reasoned that if these proteins were necessary for entry into cells, reduction of their levels should diminish infection by Ebola. However, they observed little effect on Ebola virus infection when they reduced levels of expression of all three Tyro3 family genes. They therefore concluded that it is unlikely that this family of proteins is the sought-after entry factor for Ebola virus. They have since switched to a different tactic, known as a negative genetic screen, in an attempt to identify the cellular receptor that Ebola utilizes to gain entry into cells. Through this work, they hope to achieve a better understanding of Ebola virus cell binding and entry, with an eye towards therapeutic intervention.
***********TOTALLY GUT WRENCHING PHOTO************
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