Replication Of Hev Is Still Largely Unknown Because Effective Cell Culture System For Hev

Viruses are microscopic particles that invade and take over both eukaryotic and prokaryotic cells. They consist of two structures, which are the nucleic acid and capsid. The nucleic acid contains all genetic material in the form of DNA or RNA, and is enclosed in the capsid, which is the protein coating that helps the virus attach to and penetrate the host cell. In some cases, certain viruses have a membrane surrounding the capsid, called an envelope. This structure allows viruses to become more stealthy and protected. There are two cycles in which a virus can go into: lytic and lysogenic. The lytic cycle consists of the virus attaching to a cell, injecting its DNA, and creating more viruses, which proceed to destroy the host. On the other hand, the lysogenic cycle includes the virus attaching to the cell, injecting its DNA, which combines with the cell’s DNA in order for it to become provirus. Then, the provirus DNA may eventually switch to the lytic cycle and destroy the host.

consists of two types; HSV1 and HSV-2, both of which infect humans and are easily

HeLa simply stands for Henrietta Lacks, a young mother in the 1951 who went to the doctor complaining of vaginal bleeding and discovered she had cervical cancer. Henrietta’s cells were taken for a biopsy and were found to be like nothing ever seen before; her cells were immortal. Her cancer cells double every 20 to 24 hours and have lived on for the past 60 years. Since HeLa cells were created, our world of modern medicine has been completely changed. We now vaccines for once incurable diseases and have used the cells for cloning and other biomedical research. Although the cells have done a great deal of good,

RSV enters a cell through fusion at the plasma membrane. Initiation emerges when the G protein of the RSV binds to a specific long unbranched polysaccharide of the

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.

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

Historically, in medical research, researchers have taken patients cells or organs and used them for research without their consent. Occasionally there are connections with a lack of consent and the economic, social and educational ranking of the patient being used for medical research. There have been trends that show the medical community has taken advantage of the less educated, they may not understand what is happening and/or all the risks involved. Consent should be required at the same level for all patients regardless of their status in society or level of education.

To further prove that TRIM5α was responsible for restricting HSV replication, TRIM5α expressing HeLa (H-R) cells were used to observe whether or not there was a reduction in replication and compared it to control HeLa (H-L) cells. It was found that low MOIs resulted in successful TRIM5α restriction of replication, but higher MOIs resulted in similar results in H-R and H-L cells. The viral yield was measured on Vero cells. This is an interesting result because both the H-R cells and H-L cells could not reduce replication of the virus with a high MOI. This might have to due with the amount of TRIM5α in the H-R cells and the virus can easily overwhelm at a certain threshold.

Some viruses also have an outer bag of lipo-protein called an envelope. After a virus attaches to a living cell, it either enters the cell to release the genetic information, or, the virus injects the information through the cells outer lining. Thus changing the cells natural functions and forcing the cell to spend its energy to create copies of the virus. The cell will go on making copies of the virus until the cell is used up and dies. The virus then leaves the dead cell and invades a nearby cell and the process starts all over. There are five types of human herpes virus: Varicella zoster which causes chickenpox, Epstein Barr virus which causes infectious mononucleosis, cytomegalovirus which can cause cytomegalic inclusion disease in infants, and herpes simplex viruses 1 and 2.

Every person and thing in this world is affected by Henrietta Lacks’s cells called HeLa cells. All of the cells originated from Henrietta’s cervix where a cell biologist named Gey took a sample of Henrietta's tumor without her consent. When Gey’s assistant, Mary Kubicek, is given the cells, she believes them to be just like any other cells and doesn't wish to go into deeper examination. Once she comes back to her cubicle the next day to see that the cells have multiplied in great amounts, she is astonished. These cells are used for anything and everything such as curing diseases and creating vaccines. Not only are they used for diseases and vaccines, but they are also used for cosmetics and pharmaceuticals. The cells are used to test the safety

Before the HeLa cell line, scientists struggled to keep human cells alive for more than a couple days, which was necessary for their research of how human cells function, disease develop, and testing vaccines and treatments. In 1951, the HeLa cell was discovered by Dr. George Gey, a scientist at John Hopkins University, which proved to be an immortal cell line that has the ability to regenerate and create endless copies of the original cells. Unlike other cells that tend to die after about 50 divisions the HeLa cells have the ability to continuously keep growing. Dr.Gey had been searching to find an immortal cell line, when he came across the tumors of a patient with cervical cancer named Henrietta Lacks. Henrietta Lacks was a black woman from

GAGs and the LDL-R may facilitate initial attachment to the host cell. This interaction is probably mediated by the lipoproteins associated with HCV virions. However, one cannot exclude direct contact between HCV envelope proteins and these cellular proteins. After the initial binding step, the particle likely interacts with SR-BI and CD81. HCV E2 binds with high affinity to the large external loop of CD81 andCLDN1 acts at a late stage of the entry process (Helle and Dubuisson, 2008).

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

HCMV is capable of infecting an extensive range of cell types in vivo. According to Compton (2004), the infection of a fibroblast begins with an initial tethering of a virion to cell surface - heparan sulfate proteoglycans. Then the HCMV glycoprotein, gB, is directly fused to cellular receptors such as epidermal growth factor receptor (EGFR) and cellular integrins occurs at neutral pH (Compton, 1992). The fusion with the envelope is followed by attachment of the virion and release into the cytoplasm (Roizman & Pellet, 2001). HCMV entry into epithelial and endothelial cells occurs through endocytosis in a low-pH condition (Ryckman et al., 2006) using the viral glycoproteins UL131-128 (Hahn et al., 2004). Infected cells show several

HSV-1 is a double stranded DNA virus. It being a herpes virus it is a member of the alpha-herpesvirus group, meaning its primary agent of recurrent is facial herpetic lesions. The structure of HSV-1 is composed of a capsid, a tegument, and a membrane envelope. The capsid is icosahedral, and contains seven proteins. These seven proteins are VP5, the capsomers, VP19C and VP23 the triplexes, VP26 hexon tips, UL 25 which have five near each penton, Ul17 which also have five near penton, and the portal a unique vertex. VP5 is the major capsid protein, which are the subunits of the capsomers, both the hexons and the pentons. There are 162 capsomers that creates the outer shell of the capsid. The triplexes are composed of VP19C and VP23. The portal proteins are important because they form a ring at the