The Ebola virus (EBOV) Essay

Ebola is the virus Ebolavirus (EBOV), a viral genus, and the disease Ebola hemorrhagic fever (EHF), a viral hemorrhagic fever (VHF). The virus is named after the Ebola River Valley in the Democratic Republic of the Congo (formerly Zaire), which is near the site of the first recognized outbreak in 1976 at a mission hospital run by Flemish nuns. It has remained largely obscure until 1989 when several widely publicized outbreaks occurred among

The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.

The SH (small hydrophobic) protein, matrix protein (M), and the M2 protein are envelope-associated proteins that are not involved in viral attachment or syncytium formation (3). Other proteins such as the nucleoprotein (N), phosphoprotein (P), and the large nucleoprotein (L) are in the nucleocapsid. NS-1 and NS-2 are non-structure protein that is only found in the infected cells but not present in virions (3).

Step 1: How will you identify the “vital” cellular protein that the virus targets for degradation? (Hint: think proteomics). (3 pts.)

As with any infectious disease, whether it originates from a virus, bacterium, or fungi, there is the possibility that it will become an epidemic. For centuries, deadly diseases have threatened to infect and possibly eradicate mankind. The Ebola virus, which causes an extremely fatal hemorrhagic fever, is considered to be one of the most aggressive contagions in the world. The Ebola virus is a member of a family of RNA viruses known as, “Filoviridae” and is composed of multiple distinct subspecies (Bausch et al. 2007). It causes Ebola Virus Disease, a fairly new disease that plagues multiple poor countries within Africa. The virus mainly attacks the lymphatic system, but also severely damages the reproductive and reticuloendothelial systems. The Ebola virus disease causes muscle pain, weakness, limited kidney and liver function and extreme blood loss due to failure of blood clotting.

got sick and died. This outbreak infected 318 with a death rate of 93% (Le

Cell Bio Bites Topic: How do viruses access the nucleus? Blocking nuclear import and the fight against HIV

These virus replicates in the cell nucleus. The cell mediated immunity plays a role in preventing the replication and controlling the infection caused by these viruses.

The Ebola Virus is an extremely deadly virus found in Africa. There have been multiple outbreaks across Africa and one in the United States. The Ebola virus basically causes uncontrollable bleeding externally and internally. Then your organs become liquefied. This usually results in death(www.encyclopedia.com). The following report contains info on the characteristics and history of the Ebola Virus.

Replication pattern of HEV is still largely unknown because effective cell-culture system for HEV has been developed recently (Tanaka et al., 2007). It is believed that HEV enters the cell by binding to cellular receptor, heparin sulfate proteoglycans (HSPGs), with its capsid protein and viral entry is carried out by the binding of C-terminal region of ORF2 to the cell surface protein, heat shock cognate protein 70 (HSC70) (Zhou and Emerson, 2006; Kalia et al., 2009). Also, p239, a truncated partial homodimer of the HEV capsid protein (HEV239) potentially binds to the HEV receptor(s) on cells (He et al., 2008) and a cellular chaperone, glucose regulated protein (Grp78) (Yu et al., 2011). However, more studies should be conducted to confirm the cellular receptors for HEV. The mechanism of uncoating of the HEV genome after its entry into the cells is also unknown. One of the study has suggested that heat shock protein (HSP90) might be playing role in intracellular transport of HEV since the inhibition of HSP90 blocked the intracellular transport of the HEV239 capsid protein but did not affect the binding and entry of the truncated capsid protein (Zheng et al., 2010).

Under a microscope, Lyssavirus looks like a bullet shaped porcupine. The virus is a negative-sense, single-stranded RNA, approximately 180 nm in length and 75 nm wide. (8) The genome includes five proteins: L (transcriptase), N (nucleoprotein), NS (transcriptase-associated), matrix protein (M) and a lipid-containing envelope. (8) Together, these proteins perform various roles within the ribonucleoprotein (RNP) complex and the viral envelope. Combined with the viral RNA, the N, L, and NS proteins form the RNP complex. (8) The M protein allows viral budding (helping the virus to exit the host cell) and gives rabies its bullet-shaped morphology (physical form). (8) The G protein produces virus-neutralizing antibody (which help defend the cell from the host’s immune system). The G protein also surrounds the viral envelope with spikes that assist with attachment to other cells. (8) The internal ribonucleokapsid is helical (three dimensionally curved) in shape and includes the proteins N, polymerase L and P. This

The Ebola Haemorrahagic Fever, or Ebola for short, was first recognized as a virus in 1967. The first breakout that caused the Ebola virus to be recognized was in Zaire with 318 people infected and 280 killed. There are five subtypes of the Ebola virus, but only four of them affect humans. There are the Ebola-Zaire, Ebola-Sudan, Ebola-Ivory Coast and the Ebola-Bundibugyo. The fifth one, the Ebola-Reston, only affects nonhuman primates. The Ebola-Zaire was recognized on August 26, 1976 with a 44 year old schoolteacher as the first reported case. The Ebola-Sudan virus was also recognized in 1976 and was thought to be that same as Ebola-Zaire and it is thought to have broken out in a cotton factory in the Sudan. The Ebola-Ivory Coast was

The protective capsid helps the virus escape detection and destruction during the invasion of the host. When the virus reaches the target cell, biochemical reactions between the capsid and cell wall allow the virus to latch on and inject its genome into the cell’s interior. Once inside, the viral genetic material insinuates itself into the host’s DNA or RNA. In an efficient feat of natural bioengineering, the host cell’s genetic machinery now does the rest of the work for the virus. The cell, which had already been making copies of its own genome, now also replicates that of the virus. Coded within the viral material is the blueprint for making more copies of the viral genome. Further instructions command the production of capsids and directions for assembly of new viruses. After the host cell becomes engorged with viruses, it explodes, sending the new

The HIV-1 virion is approximately 120 nm in diameter, roughly spherical, and is composed of two copies of a single stranded positive sense RNA enclosed by a capsid (24). The HIV-1 genome is less than 10 kb and encodes for more than nine different gene products. It encodes for 3 major structural protein genes: gag (group-specific antigen), pol (DNA polymerase), and env (Envelope), which code for major structural proteins and essential enzymes. Gag generates the mature Gag protein matrix (MA or p17), capsid (CA or p24), nucleocapsid (NC or p7), and p6, which encompass proteins for the basic infrastructure of the virus such as the inner core of the viral particle (25). Pol encodes for reverse transcriptase (RT), which enables the virus to reproduce, integrase (IN), which is necessary to integrate the viral double stranded DNA into the host genome, RNAse H, and HIV protease, which are all encapsulated in the core of the inner particle formed by the viral capsid protein p24 (25). Env encodes for glycoproteins of the outer membrane such as outer gp120 (which enables the virus to attach and fuse to cells of the host), and transmembrane gp41 that anchors the glycoprotein complex to the surface of the virion (25). Between the core and the envelope is the HIV matrix proteins which are composed of the viral protein p17 (23). HIV-1 also encodes for proteins with important regulatory elements (tat (Trans-Activator of Transcription) and rev

Specific Aim 2: Explore the role of RNA interaction interface residues in ICP27 function during viral infection. This specific aim will be performed in collaboration with Dr. Alexander Golovanav and will investigate the phenotype of ICP27 recombinants with mutated RNA interface residues within the RGG motif.