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Ebola virus em

An electron micrograph of an Ebola viral particle showing the characteristic filamentous structure of a Filoviridae. The viral filaments can appear in images in various shapes including a 'u', '6', a coil, or branched resulting in pleomorphic particles. The filaments are reported to be between 60-80 nm in diameter, the length of a filament associated with an individual viral partial is extremely variable with Ebola particles of up to 14,000 nm in length being reported. An average length, which may represent the most infectious particles is in the region of 1000 nm. The first electronmicrograph of Ebola was 13 October 1976 by Dr. F.A. Murphy, now at UC Davis, who was then working at the CDC. The nucleocapsid structure consists of a central channel, 20-30nm in diameter, surrounded by helically wound capsid with a diameter of 40-50nm and an interval of 5nm. 7nm glycoprotein spikes spaced 10 nm apart from each other are present within the outer envelope of the virus which is derived from the host cell membrane. Each viral particle contains one molecule of single-stranded, negative-sense RNA, which encodes the seven viral proteins.

The virouses involved[]

Ebola[]

The genus Ebolavirus is a virological taxon included in the family Filoviridae, order Mononegavirales. The members of this genus are called ebolaviruses.

The five known virus species are named for the region where each was originally identified: Bundibugyo ebolavirus, Reston ebolavirus, Sudan ebolavirus, Taï Forest ebolavirus (originally Côte d'Ivoire ebolavirus), and Zaire ebolavirus. The Ebola viral protein 24 (eVP24) inhibits interferon type I and type II signaling by binding to NPI-1 subfamily karyopherin α (KPNA) nuclear import proteins, preventing their interaction with tyrosine-phosphorylated STAT1 (phospho-STAT1). This inhibits phospho-STAT1 nuclear import. A biochemical screen now identifies heterogeneous nuclear ribonuclear protein complex C1/C2 (hnRNP C1/C2) nuclear import as an additional target of eVP24. Co-immunoprecipitation studies demonstrate that hnRNP C1/C2 interacts with multiple KPNA family members, including KPNA1. Interaction with hnRNP C1/C2 occurs through the same KPNA1 C-terminal region (amino acids 424–457) that binds VP24 and phospho-STAT1. The ability of hnRNP C1/C2 to bind KPNA1 is diminished in the presence of eVP24, and cells transiently expressing eVP24 redistribute hnRNP C1/C2 from the nucleus to the cytoplasm. These data further define the mechanism of hnRNP C1/C2 nuclear import and demonstrate that the impact of eVP24 on nuclear import extends beyond STAT1.

Each species of the genus Ebolavirus has one member virus, and four of these cause Ebola virus disease (EVD) in humans, a type of hemorrhagic fever having a very high case fatality rate; the fifth, Reston virus, has caused EVD in other primates. Zaire ebolavirus is the type species (reference or example species) for Ebolavirus, and has the highest mortality rate of the ebolaviruses, and is also responsible for the largest number of outbreaks of the five known members of the genus, including the 1976 Zaire outbreak and the outbreak with the most deaths (2014).

Ebolaviruses were first described after outbreaks of EVD in southern Sudan in June 1976 and in Zaire in August 1976. The name Ebolavirus is derived from the Ebola River in Zaire (now the Democratic Republic of the Congo), the location of the 1976 outbreak, and the taxonomic suffix -virus (denoting a viral genus). This genus was introduced in 1998 as the "Ebola-like viruses". In 2002 the name was changed to Ebolavirus and in 2010, the genus was emended. Ebolaviruses are closely related to marburgviruses.

The Ebola virus (/ɛˈboʊlə/; EBOV, formerly designated Zaire ebolavirus) is one of five known viruses within the genus Ebolavirus. Four of the five known ebolaviruses, including EBOV, cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD). Ebola virus has caused the majority of human deaths from EVD, and is the cause of the 2013–2015 Ebola virus epidemic in West Africa, which has resulted in at least 28,616 suspected cases and 11,310 confirmed deaths.

Ebola virus and its genus were both originally named for Zaire (now the Democratic Republic of Congo), the country where it was first described, and was at first suspected to be a new "strain" of the closely related Marburg virus. The virus was renamed "Ebola virus" in 2010 to avoid confusion. Ebola virus is the single member of the species Zaire ebolavirus, which is the type species for the genus Ebolavirus, family Filoviridae, order Mononegavirales. The natural reservoir of Ebola virus is believed to be bats, particularly fruit bats, and it is primarily transmitted between humans and from animals to humans through body fluids.

The EBOV genome is a single-stranded RNA approximately 19,000 nucleotides long. It encodes seven structural proteins: nucleoprotein (NP), polymerase cofactor (VP35), (VP40), GP, transcription activator (VP30), VP24, and RNA-dependent RNA polymerase (L).

Because of its high mortality rate (up to 83-90%), BOV is also listed as a select agent, World Health Organization Risk Group 4 Pathogen (requiring Biosafety Level 4-equivalent containment), a U.S. National Institutes of Health/National Institute of Allergy and Infectious Diseases Category A Priority Pathogen, U.S. CDC Centers for Disease Control and Prevention Category A Bioterrorism Agent, and listed as a Biological Agent for Export Control by the Australia Group.

Marburg virus[]

The genus Marburgvirus is the taxonomic home of one species, Marburg marburgvirus, whose members are the two known marburgviruses, Marburg virus (MARV) and Ravn virus (RAVV). Both viruses cause Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever, and both are Select Agents, World Health Organization Risk Group 4 Pathogens (requiring Biosafety Level 4-equivalent containment), National Institutes of Health/National Institute of Allergy and Infectious Diseases Category A Priority Pathogens,[4] Centers for Disease Control and Prevention Category A Bioterrorism Agents, and are listed as a Biological Agents for Export Control by the Australia Group.

Marburg virus is a hemorrhagic fever virus of the Filoviridae family of viruses and a member of the species Marburg marburgvirus, genus Marburgvirus. Marburg virus (MARV) causes Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever. The virus is considered to be extremely dangerous. The WHO rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment). In the United States, the NIH/National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.

The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected copulation and broken skin. The disease can cause bleeding (haemorrhage), fever and other symptoms much like Ebola. Funeral rituals are a particular risk. Actual treatment of the virus after infection is not possible but early, professional treatment of symptoms like dehydration considerably increase survival chances.

In 2008, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala, Uganda.

The treaty[]

Until 1998, the family Filoviridae contained only one genus, Filovirus.Once it became clear that marburgviruses and ebolaviruses are fundamentally different, this genus was abolished and a genus "Marburg-like viruses" was established for marburgviruses. In 2002, the genus name was changed to Marburgvirus, and in 2010 and 2011 the genus was emended.

The Switzerland, Norway, Egypt, Angola, Brazil, Sudan, USA, Texas, Louisiana, Florida, Canada, Quebec, New England, Queensland, Liberia, Nigeria, Peru, India, Vietnam, China, Japan, Ireland, Poland, Prussia, Portugal, California, Cuba, Brazil, Spain and France all expressed thire concerns at the UN about the largely lethal various outbreaks that had occurred in recorded history and wished the world would take the situation more seriously.

These nations pushed for debate and research on the issue at every opportunity over the next 3 years and finally got a serious debate going by 2006. The nations of the world the all signed the Third Zürich World Health Treaty in 2006, which made it a global priority to do research into a vaccine for it and an international obligation to help any nations that reported a outbreak before it became a major global health concern. The treaty was chaired and hoasted by the Swiss.

Related UN treaties[]

  1. First Zürich World Health Treaty (A better world TL)
  2. Second Zürich World Health Treaty (A better world TL)
  3. Third Zürich World Health Treaty (A better world TL)
  4. Zürich Ozone Hole Treaty (A better world TL)
  5. Zürich Hydrofluorocarbons Treaty (A better world TL)
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