Ebola virus (EBOV)
Introduction
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Ebola virus (EBOV) is a member of the Filoviridae virus family along with Marburg virus (MARV). Together they are commonly known as filoviruses. EBOV is a virulent pathogen that causes fatal hemorraghic fever in humans and nonhuman primates (Hartlieb et al 2005). A large majority of patients infected with EBOV, and who are not properly treated, die within five to seven days after exposure (Leroy et al. 2000). There has been greater than 2,300 reported cases of hemmorraghic fever caused by filoviruses, EBOV and MARV (Yermolina et al. 2010). This number is expected to be even higher as it is expected that many cases go unreported in rural African villages. Not only has this viral pathogen affected human populations, but has also aided in the decline of western gorilla populations near central Africa (Yermolina et al. 2010).
The genome of this fatal pathogen possesses a linear non segmented single negative-stranded RNA, and codes for seven structural proteins, which include: nucleoprotein (NP), VP35, VP40, glycoprotein (GP), VP30, VP24, and L protein, which provides RNA-dependent RNA activity (Leroy et al. 2000). These structural proteins are the primary targeted sites of vaccines in many current studies as they are vital sites for silencing EBOV outbreaks. There are currently five species of the infectious virus that differ from each other by 37-41% based on their amino acid and nucleotide sequencing (Jones et al. 2005). This fluctuation is amino acid and nucleotide sequencing leads to a large problem in finding a cure as vaccinations for one species does not guarantee vaccination for any other species. The five species include: Zaire ebolavirus (ZEBOV), Sudan ebolavirus (SEBOV), Reston ebolavirus (REBOV), Ivory Coast ebolavirus (CIEBOV), and the newly found Bundibugyo ebolavirus species, which was discovered in the most recent outbreak in 2007 (Jones et al. 2005). Of the five species ZEBOV is cited to be the most lethal strain with up to 90% mortality rate (Geisbert et al. 2010). EBOV outbreaks are commonly found throughout central Africa, although they are not constrained to this area as they easily and rapidly spread.
There are many symptoms involved with the onset of EBOV. The first mild symptoms include: fever, fatigue, anorexia, malaise, myalgia, severe frontal headache, and pharyngitis. These preliminary symptoms are able to last two to sevens days. As the virus continues to spread throughout the patient the symptoms continue to get worse as melena, epistaxis, confusion, hearing loss, and maculopopular rash begins to form, which is then followed by vomiting and bloody diarrhea. The final characteristic of EBOV is uncontrollable haemorrhage, which leads to death as victims fall into shock related to the amount of blood lost (Cohen 2004 and Ledgerwood et al. 2011). The first recorded outbreaks of EBOV were in 1976, as two outbreaks of different strains occurred. The outbreaks arose in northern Zaire and caused a 90% mortality rate, and the other outbreak occurred in southern Sudan and resulted in a 50% mortality rate (MICROBEWIKI WEBSITE). Since these initial outbreaks there have been 25 more EBOV outbreaks, of which four were epidemic (CDC website). The first EBOV vaccine used on nonhuman primates consisted of a DNA prime-adenovirus boost approach (Jones et al. 2005).Vaccination techniques have greatly altered form this first attempt and have displayed much more efficient apothegenic results.
Transmission and Reproduction
Ebola virus (EBOV) is fatal to Africa as the majority of major outbreaks have emerged from central Africa. EBOV is not only a dangerous virus because it is a virulent pathogen, but also because it spreads rapidly as this virus is easily transmitted between individuals. It is still unclear how the virus first began to spread, but it is believed that humans incidentally obtained the virus from direct contact with contaminated animal, which are usually dead carcasses (Ledgerwod et al. 2011). There is an increased belief that cave dwelling fruit bats are a reservoir for EBOV as evidence of asymptomatic infection has been confirmed in three species of these fruit bats (Ledgerwood et al. 2011). The most common way the virus is spread is through direct contact with an infected individual, whether human or nonhuman primate (Hartlieb et al. 2005). The virus is transmitted contact with bodily fluids, blood or tissue. It is also commonly transmitted in third world hospital environments where contact with infected bodily fluid is common. This commonly occurs through reuse of unsterilized contaminated needles and syringes which increases the spread of the viral pathogen (Jaax et al. 1995). EBOV most frequently enters individuals through openings in the skin, such as cuts or scrapes, as well as through the gastrointestinal tract, and conjunctiva (Johnson et al. 1994).
Along with these natural forms of transmission, other studies have found an unnatural transmission of the virus through the air. Aerosol transmission was first discovered in 1992 during an EBOV outbreak. Monkeys located in a quarantine facility quickly all became infected with EBOV even though they were separated from each other in individual cages (Johnson et al. 1994). Shortly after it was determined that EBOV is capable of unnaturally being transmitted by aerosol, which has displayed high rates of infection when it is inhaled as particles in the air (Leffel et al. 2004). Based on these terrifying results EBOV, along with MARV, have been categorized as category A biological weapons, and as a possible threat of bioterrorism (Leffel et al 2004, Yermolina et al. 2010). This has lead to large scare as there is currently no vaccine for EBOV.
EBOV has an encapsulated negative-stranded RNA genome that is 19 kb long and codes for seven structural proteins. These seven proteins include: nucleoprotein (NP), VP35, VP40, glycoprotein (GP), VP30, VP24, and L protein, which provides RNA-dependent RNA activity (Leroy et al. 2001). A large breakthrough in recent studies was the discovery that EBOV, like other viruses, uses host cellular protein machinery to assemble viral replicants, and to bud new copies of the virus from the host cell membrane as EBOV reproduces asexually inside of the host cell (Hartlieb et al. 2005). Of the seven structural proteins, VP40 is the major structural protein as it is composed of vital information for the replication process, including assembly and budding of new viral copies (Hartlieb et al. 2005). An imperative process for viral replication is RNA binding, and therefore octamer formation (Hoenen et al. 2005). The envelope of EBOV is covered in many GP, which is a transmembrane protein, and binds to the host cell membrane. Binding to the host cell membrane allows the virus to freely enter into the cytoplasm of the host cell (Hartlieb et al. 2005). Once the GP binds to the host cell the viral membrane fuses with the host cell membrane allowing the viral particles to be released into the host cytoplasm (MICROBEWIKI). Once the viral parts enter the host cell, EBOV VP40 is transported from the endosome to the plasma membrane via the retrograde late endosomal pathway by means of multi-vesicular bodies (MVBs) (Hartlieb et al. 2005). Once located in the plasma membrane VP40 is able to localize viral assembly and budding machinery, from the host, with the help of Tsg101 and HECT domain (Hartlieb et al. 2005). GP then re-localizes to MVBs and transported to the site of assembly and budding on the plasma membrane (Kolesnikova et al. 2004). NP becomes expressed and forms intracellular inclusion bodies (Hartlieb et al. 2005). NP determines the structure of the nucleocapsid, and recruits VP30, VP35, and L protein into the inclusion bodies in the nucleocapsid (Becker et al. 1998). Once all the protein structures are in place budding of new viral copies begins (Hartlieb et al. 2005). This is a very rapid process as many untreated patients die within 5-7 days after exposure to this lethal pathogen (Hartlieb et al. 2005).
Section 2
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Section 3
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Conclusion
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References
Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2009, Kenyon College.
