Unlike animals and plants, which also use DNA as a repository of information, viruses are not technically alive because they are incapable of replicating without help. In order to get into the cell, Ebola must travel through the cell membrane, which is a barrier that protects the cell from its environment.
However, all cells need nutrients, which must have ways of entering the cell; the viruses hitch a ride into the cell via one of these established nutrient-uptake entryways. B Ebola has a protein called glycoprotein that sticks out of its membrane and binds to receptors in red on the cell surface. Ebola virus is characterized by a variety of symptoms, beginning with fever, headache, and muscle pain, followed by vomiting, diarrhea, and internal bleeding [3].
Upon entering the body, the virus targets specific cell types, including liver cells, cells in the immune system, and endothelial cells, which line the inside of blood vessels. Once inside the cells, one of the proteins made by the virus is called Ebola virus glycoprotein [4]. The glycoprotein can disrupt cell adhesion, so that cells have trouble sticking to each other and to a scaffold called the extracellular matrix, which in healthy tissue helps to hold the cells together. The loss of cell adhesion is detrimental to any solid tissue, and by infecting blood vessel cells, the virus causes the vessels to become leaky, leading to hemorrhaging and internal bleeding.
Over time, infection of cells throughout the body can cause organ failure, while fever, internal bleeding, diarrhea and vomiting can cause severe loss of electrolytes, blood plasma, and fluid. Ultimately, organ failure and shock caused by the internal bleeding lead to death [5]. Researchers are exploring several avenues for treating Ebola.
Many drug companies are developing vaccines, although none of these vaccines is ready for full-scale production, or even approved for human treatment [6]. These vaccines use non-virulent portions of the virus injected into the body, to teach the immune system to recognize the Ebola virus and defend your body against it in the event of a true infection. Although the vaccines would usually be months or even years away from approval, emergency protocols approved by the World Health Organization have determined that this epidemic warrants the use of unapproved drugs and vaccines, so cautious plans are being made to expand access to Ebola victims [7,8].
Another treatment which has been used for several health-care workers who became infected with Ebola virus involves the use of antibodies.
Antibodies are large, Y-shaped proteins that are designed to recognize and neutralize foreign objects in your body, such as bacteria or viruses. Currently, the most well developed drug is called ZMapp, which is a cocktail of three antibodies. Retrieved November 10, from www.
A Singapore study has A new study shows that infection sites could affect the immune system's response to a Initially targeting cells of the immune system called macrophages, white blood cells that absorb and clear away What is not well known is that the virus also can ScienceDaily shares links with sites in the TrendMD network and earns revenue from third-party advertisers, where indicated.
Print Email Share. Just a Game? Living Well. Ebola virus EBOV belongs to the family of filoviruses which include seven viral species. Currently, eight virus types have been identified within this virus family [ 1 ]. The virus particles have a uniform diameter of 80 nm but can extend even up to 10, nm [ 2 ].
In humans EVD is characterized by a severe disease with high fever, diarrhea and vomiting, occasionally hemorrhagic manifestations, and suppressed immune and inflammatory responses which often lead to sepsis-like symptoms and hypovolemic shock [ 5 ]. Because of its high case-fatality rate and limited treatment and vaccination options, EBOV is classified as a biothreat pathogen of category A [ 6 ] and should be handled at biosafety level 4 BSL-4 laboratories.
EBOV is also considered as one of the deadliest human pathogens and a potential bioterrorism agent [ 7 ]. EBOV infection targets many tissues and cell types leading to dysregulation of inflammatory mediators, disrupted homeostasis, and impaired host immune responses.
Together with abnormalities in the coagulation and vascular system, the infection often leads to a fatal outcome in humans due to a multiorgan failure [ 8 , 9 , 10 ]. Invading and replicating viruses are recognized by the host via cellular pattern recognition receptors PRRs.
PRRs recognize pathogens via pathogen-associated molecular patterns PAMPs , such as viral structural components and nucleic acids, which then activate host innate immune responses. The produced interferons are important in activating the second phase of innate immune responses in epithelial cells, fibroblasts, leukocytes, or basically any cell that has functional IFN receptors.
Single-stranded viruses with negative-sense RNA genomes can be assigned to three different subgroups whether they are multisegmented, circular, or unsegmented [ 18 ]. Unsegmented viruses belong to the order of Mononegavirales , and the filovirus group is one of the eight mononegaviral families [ 19 ].
Filoviruses are enveloped, non-segmented, negative-stranded RNA viruses of varying morphology. They are called filoviruses because of their filamentous particle structure [ 20 ]. Most of the filoviruses are human pathogens, and the diseases caused by two of these viruses, EBOV and MARV, are well-known because of their high case-fatality rate [ 3 ].
Filoviruses consist of ssRNA genomes of 19 kilobases. EBOV genome encodes eight different proteins that all have specific functions [ 22 ]. Table 1 summarizes the major characteristics of EBOV proteins. Nucleocapsid-associated proteins include the major nucleoprotein NP and the minor nucleoprotein VP Ribonucleoprotein complex regulates viral replication and transcription of the viral genome.
VP40 is required for viral particle formation, and it is the major matrix protein [ 27 ]. Viral envelope glycoprotein GP is the only viral envelope protein, and its function is to attach the host cell surface and mediate the entry of viral nucleocapsids [ 28 ]. On the surface of virus particles, GP is cleaved into two subunits GP1 and GP2 , and it exists as a trimeric protein complex peplomers.
The viral genome encodes also VP24 which is a minor matrix protein, and its functions are dealing with virion assembly and downregulation of host innate immune responses see below. Ebola virus proteins and their functions in virus replication cycle and in host cell functions. Ebola virus genome structure and the expression of individual EBOV proteins in transfected cells.
Panel A. Panel B. Note that VP40 and especially VP24 are localized into the cell nucleus, and GP-expressing cells show significant cytotoxicity. EBOV can infect a wide variety of cells, which may explain the ability of the virus to spread to many tissues and different types of cells. At present there is no direct evidence of one specific EBOV receptor; rather many types of molecules such as integrins, C-type lectins, and TIM-1 have been suggested to function as a cellular receptor.
After attachment EBOV is endocytosed followed by a fusion of viral and endosomal membranes and release of viral nucleocapsid into the cell cytoplasm. Both the transcription and translation of EBOV proteins takes place in the cell cytoplasm. GP synthesis and glycosylation occurs in the Golgi complex, and the assembly of newly produced virus particles takes place at the plasma membrane where NCs, VP40, VP24, and GP are assembled followed by virus budding from the plasma membrane [ 22 , 23 , 24 , 25 , 26 , 27 ].
Ebola virus disease was first recognized in simultaneously in two different geographic locations, in Sudan and in the Democratic Republic of Congo [ 9 , 30 ]. The newly identified viral agent was named Ebola virus, and the symptoms resembled those of Marburg virus disease MVD. Like in many other zoonotic diseases, EBOV is considered to have a natural reservoir in animals, but humans may also transmit the disease via blood, serum, and bodily secretions Figure 2. Patients that recovered from the primary infection were found to excrete the virus for several weeks or months also via the genital tract, especially in semen [ 31 ].
Humans and possibly some other mammalian species like primates are considered as the dead-end hosts [ 32 ]. Even though there are no firm links to natural reservoirs of EBOV, many studies suggest that rodents and bats likely play a role in virus transmission [ 33 , 34 , 35 , 36 ]. There is strong evidence that fruit bats, in case they are in close contact with humans or when they are used as food, transmit the disease to humans. EBOV may exist silently in reservoir species and be activated through certain stimuli such as stress, coinfection, pregnancy of the carrier animals, ecological changes, and change in food habits [ 37 , 38 ].
0コメント