HCV Entry Essay

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.

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

Ans) – The usual causes of hep C is coming in contact with infectious fluids and seretions from

Hepatitis C virus (HCV) is from the virus family Flaviviridae with an RNA envelope serving as it's genetic material. The genetic material (RNA) is HCV's pathogenic structure. The genome is positive sense single stranded RNA, which is very similar to mRNA and can be translated quickly to the host cell (Bauman 2012). Hepatitis C is an enveloped virus, and the RNA also lacks a proofreading ability after replication, which results in mutations coding for many genotypes within the host. This genetic variability makes it difficult for the host immune system to clear all the HCV infections. As one infection clears, another strain is being produced (Bauman 2012). The HCV antibody detected by ELISA(Wilkinson

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).

HSV is a human nuclear DNA virus that can replicate in many different species of animal as well as in many different types of cells. It can gain access to different types of cells due to its 12 envelope surface glycoproteins and uses the heparan moiety of the receptors to attach to cells

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.

On March 24th at 7:30 in the Chapel, Jay Parish presented “The Discovery of Antiviral Agents and What I Learned Learned Along the Way”. He elaborated on his contributions to the study of anti-virals for the treatment of different viruses, particularly Hepatitis C. By explaining the course of the virus, Mr. Parish brought light to a medical concern that is typically unheard of by people. His lecture was quite interesting in that it made people realize that the parameters of an illness/virus is much more complex than perceived.

When a virus invades the human body there is an assortment of responses from the immune system relying largely on the particular pathogen type. Viruses invade the host with the purpose of replication to ensure survival. My cytosolic virus is a single stranded RNA virus. The virus is surrounded by an envelope with a lipid membrane. Inside the envelope are matrix proteins, integrase, protease, reverse transcriptase and the RNA genome. All viruses contain three proteins necessary for their survival; one for replication, one for packaging and delivering it to more host cells and a protein that modifies the function or structure of the host

The immune response against HSV involves both innate and adaptive immune mechanisms. They both play pivotal role in mediating the immune responses and controlling viral pathogenesis. The first line of defence is comprised of components of innate immunity, such as various cytokines, natural killer (NK) cells and dendritic cells (DCs), which all dispense antiviral activities in eradicating the infection (Wakimoto et al., 2003). The key players of the adaptive immunity are B and T cells, which generate pathogen-specific immune response and thus control the spread of infection (Harandi et al., 2001; Kwant-Mitchell et al., 2009).

Although we are well aware of the mode of transmission, the hepatitis C virus itself remains a mystery. The genome of HCV is extremely mutable. Because HCV is an RNA virus and does not have adequate proofreading ability as it replicates, virions infecting humans undergo evolution with time, giving rise to the notion that HCV persists as a collection of virus quasispecies. Because it is constantly mutating, HCV is able to escape detection and elimination its human host. HCV undergoes quick mutation in a hypervariable region of the genome coding for the envelope proteins and escapes immune surveillance by the host. As a result, most HCV-infected people develop chronic infection. HCV also knocks out the host’s innate immunity.

Herpes simplex virus is two types HSV-1 and HSV-2. HSV-1 is responsible for orofacial infections, and HSV-2 is responsible for genital infections. In my perspective, developing HSV-2 vaccine is more important since it is one of the most sexual transmission disease(1), and it can lead to a chronic infection which increases the risk of HIV infection. It also transmits to neonates during birth, and most cases are asymptomatic. The lecture for this week mentions the most recent clinical trials for therapeutic and prophylactic vaccines against HSV-2 and to get antibodies response. The platforms were inactivated or subunit vaccines with adjuvants. Furthermore, the lecture states new Approaches that improve HSV vaccines. In my opinion, the most effective vaccine and immunity should

As mentioned earlier, HPV is a non-enveloped, icosaheadral capsid, double-stranded circular DNA virus. Infection of HPV orccurs in the cervix, glans of the penis, penile shaft, scrotom and anal verge by interactive with putative host cell surface receptors such as heparin sulfate proteoglycans and alpha-6 integrins. Most studies suggest that HPV16 enters the cell via clathrin-mediated endocytosis (Day, 2003, Bousarghin, 2003, Smith, 2007, Hindmarsh, 2007). Although a few contradictory studies suggest that HPV16 is clathrin and caveolaen independent (Spoden, 2008). The virus then uncoats and delivers its genome of 8 genes to the host cell nucleus to be expressed as autonocmous replicating episoma or extrachromasomal replication. These eight genes are named for when they are expressed during the virus’s occupation of its host: early (E) and late (L). E1,2,4 and 5 are important to genome replication, E6 and E7 are oncogenes and when unchecked can cause cancerous growth of host cell. E6 is thought to complex with p53 (Werness, 1990) which promotes the degradation of p53 via the ubiquitin pathway (Schffner et al., 1990). This degradation of p53 contributes to the oncogenic potential of high-risk HPVs. Because tt has also been shown that E6 can bind with p53 without degradation (Crook et al., 1991), it was thought that blocking E6-mediated degradation of p53 might be sufficient to reactivate p53 function. However, blocking E6-induced degradation showed that additional DNA damaging

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

Epidemiological studies have demonstrated that exposure to WBV has the potential to cause injury and is