Chris Stokely October 4 at 4:10pm · Pueblo, CO The vaccine will mutate this virus, it is raising the dead your governments lying to you, but they are dormant/ none aggressive once it mutates they will become highly aggressive for your information it is the truth. your governments trying to stop Gods plan and they are going to play God and only screw them selfs, their contingency plan is to run into underground tunnel systems, but there will be earthquakes in the near future the science is all there the underground tunnel systems are compromised by the planet its self, they need to leave the Ebola virus alone and treat it like they did with the first American that had it the black plague ran its course they need stop playing god treat the virus and not mutate it with their so called vaccine mark my words, this is not a warning it is a message. Each virion contains one molecule of linear, single-stranded, negative-sense RNA, 18,959 to 18,961 nucleotides in length. The 3′ terminus is not polyadenylated and the 5′ end is not capped. This viral genome codes for seven structural proteins and one non-structural protein. The gene order is 3′ – leader – NP – VP35 – VP40 – GP/sGP – VP30 – VP24 – L – trailer – 5′; with the leader and trailer being non-transcribed regions, which carry important signals to control transcription, replication, and packaging of the viral genomes into new virions. Sections of the NP, VP35 and the L genes from filoviruses have been identified as endogenous in the genomes of several groups of small mammals.[10][11][12] It was found that 472 nucleotides from the 3 end and 731 nucleotides from the 5 end are sufficient for replication of a viral minigenome, though not sufficient for infection.[9] The minigenomes genetic material by itself is not infectious, because viral proteins, among them the RNA-dependent RNA polymerase, are necessary to transcribe the viral genome into mRNAs because it is a negative sense RNA virus, as well as for replication of the viral genome. There are two candidates for host cell entry proteins. The first is the host-encoded Niemann–Pick C1 (NPC1), a cholesterol transporter protein, appears to be essential for entry of Ebola virions into the host cell, and for its ultimate replication.[13][14] In one study, mice that were heterozygous for NPC1 were shown to be protected from lethal challenge with mouse-adapted Ebola virus.[ambiguous][jargon][13] In another study, small molecules were shown to inhibit Ebola virus infection by preventing viral envelope glycoprotein (GP) from binding to NPC1.[14][15] Hence, NPC1 was shown to be critical to entry of this filovirus, because it mediates infection by binding directly to viral GP.[14] When cells from Niemann Pick Type C patients lacking this transporter were exposed to Ebola virus in the laboratory, the cells survived and appeared impervious to the virus, further indicating that Ebola relies on NPC1 to enter cells;[citation needed] mutations in the NPC1 gene in humans were conjectured as a possible mode to make some individuals resistant to this deadly viral disease.[citation needed][speculation?] The same studies[which?] described similar results regarding NPC1s role in virus entry for Marburg virus, a related filovirus. A further study has also presented evidence that NPC1 is critical receptor mediating Ebola infection via its direct binding to the viral GP, and that it is the second lysosomal domain of NPC1 that mediates this binding.[16] The second candidate is TIM-1 (aka HAVCR1).[17] TIM-1 was shown to bind to the receptor binding domain of the EBOV glycoprotein, to increase the receptivity of Vero cells. Silencing its effect with siRNA prevented infection of Vero cells. TIM1 is expressed in tissues known to be seriously impacted by EBOV lysis (trachea, cornea, and conjunctiva). A monoclonal antibody against the IgV domain of TIM-1, ARD5, blocked EBOV binding and infection. Together, these studies suggest NPC1 and TIM-1 may be potential therapeutic targets for an Ebola anti-viral drug and as a basis for a rapid field diagnostic assay Being acellular, viruses such as Ebola do not replicate through any type of cell division; rather, they use a combination of host- and virally encoded enzymes, alongside host cell structures, to produce multiple copies of themselves. These then self-assemble into viral macromolecular structures in the host cell.[8][better source needed] The virus completes a set of steps when infecting each individual cell:[citation needed] The virus begins its attack by attaching to host receptors through the glycoprotein (GP) surface peplomer and is endocytosed into macropinosomes in the host cell.[18][non-primary source needed] To penetrate the cell, the viral membrane fuses with vesicle membrane, and the nucleocapsid is released into the cytoplasm. Encapsidated, negative-sense genomic ssRNA is used as a template for the synthesis (3-5) of polyadenylated, monocistronic mRNAs and, using the host cells ribosomes, tRNA molecules, etc., the mRNA is translated into individual viral proteins. These viral proteins are processed, a glycoprotein precursor (GP0) is cleaved to GP1 and GP2, which are then heavily glycosylated using cellular enzymes and substrates. These two molecules assemble, first into heterodimers, and then into trimers to give the surface peplomers. Secreted glycoprotein (sGP) precursor is cleaved to sGP and delta peptide, both of which are released from the cell.[citation needed] As viral protein levels rise, a switch occurs from translation to replication. Using the negative-sense genomic RNA as a template, a complementary +ssRNA is synthesized; this is then used as a template for the synthesis of new genomic (-)ssRNA, which is rapidly encapsidated. The newly formed nucleocapsids and envelope proteins associate at the host cells plasma membrane; budding occurs destroying the cell. Ebolavirus is a zoonotic pathogen. Intermediary hosts have been reported to be various species of fruit bats ... throughout central and sub-Saharan Africa, but infection in bats has not been proven yet.[19] End hosts are humans and great apes, infected through bat contact or through other end hosts. Pigs on the Philippine islands have been reported to be infected with Restonvirus, so other interim or amplifying hosts may exist.[19] Ebola virus is one of the four ebolaviruses known to cause disease in humans. It has the highest case-fatality rate of these ebolaviruses, averaging 83% since first described in 1976, although fatality rates up to 90% have been recorded in one epidemic (2002–03). There have also been more outbreaks of ebola virus than of any other ebolavirus. The first outbreak occurred on 26 August 1976 in Yambuku.[20] The first recorded case was Mabalo Lokela, a 44‑year-old schoolteacher. The symptoms resembled malaria, and subsequent patients received quinine. Transmission has been attributed to reuse of unsterilized needles and close personal contact, body fluids and places where the person has touched. Zaire ebolavirus is pronounced /zɑːˈɪər iːˈboʊləvaɪərəs/ (zah-EER ee-BOH-lə-vy-rəs). Strictly speaking, the pronunciation of Ebola virus (/iːˌboʊlə ˈvaɪərəs/) should be distinct from that of the genus-level taxonomic designation ebolavirus/Ebolavirus/ebolavirus, as Ebola is named for the tributary of the Congo River that is pronounced Ébola in French,[21] whereas ebola-virus is an artificial contraction of the words Ebola and virus, written without a diacritical mark for ease of use by scientific databases and English speakers. According to the rules for taxon naming established by the International Committee on Taxonomy of Viruses (ICTV), the name Zaire ebolavirus is always to be capitalized, italicized, and to be preceded by the word species. The names of its members (Zaire ebolaviruses) are to be capitalized, are not italicized, and used without articles.[1] Ebola virus (abbreviated EBOV) was first described in 1976.[2][3][22] Today, the International Committee on Taxonomy of Viruses lists the virus as the single member of the species Zaire ebolavirus, which is included into the genus Ebolavirus, family Filoviridae, order Mononegavirales. The name Ebola virus is derived from the Ebola River — a river that was at first thought to be in close proximity to the area in Democratic Republic of Congo, previously called Zaire, where the first recorded Ebola virus disease outbreak occurred — and the taxonomic suffix virus.[1] The species was introduced in 1998 as Zaire Ebola virus.[23][24] In 2002, the name was changed to Zaire ebolavirus.[25][26] Ebola virus was first introduced as a possible new strain of Marburg virus in 1977 by two different research teams.[2][3] At the same time, a third team introduced the name Ebola virus.[22] In 2000, the virus name was changed to Zaire Ebola virus,[27][28] and in 2002 to Zaire ebolavirus.[25][26] However, most scientific articles continued to refer to Ebola virus or used the terms Ebola virus and Zaire ebolavirus in parallel. Consequently, in 2010, the name Ebola virus was reinstated.[1] Previous abbreviations for the virus were EBOV-Z (for Ebola virus Zaire) and most recently ZEBOV (for Zaire Ebola virus or Zaire ebolavirus). In 2010, EBOV was reinstated as the abbreviation for the virus.[1] To be considered a member of the species Zaire ebolavirus, a virus of the genus Ebolavirus is required to fulfill certain requirements:[1] it is found in the Democratic Republic of the Congo, Gabon, or the Republic of the Congo it has a genome with two or three gene overlaps (VP35/VP40, GP/VP30, VP24/L) it has a genomic sequence that differs from the type virus by less than 30% Furthermore, the virus genome cannot diverge from that of the variant Mayinga (EBOV/May) by more than 10% at the nucleotide level for it to be considered an Ebola virus.[1]
Posted on: Tue, 07 Oct 2014 20:12:34 +0000
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