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 …show more content…
In HCMV, there are four forms of capsids which are pre-B, B, C and A (Wood et al., 1996).
The development of capsids begins with the movement of capsid proteins from the site of synthesis in the cytoplasm to the nucleus where the capsid will be assembled (Gibson, 1996). The capsid shell proteins consist of major capsid protein (MCP), minor capsid protein (mCP), mCP binding protein (mC-BP), and the smallest capsid protein (SCP) (Gibson, 1996). Most of the capsid proteins are small enough to diffuse through the nuclear pores. However, the major capsid protein must merge with the assembly protein precursor (pAP) that directs the transport of the MCP/pAP complex through the nuclear pore (Figure 1.2) (Wood et al., 1996). The four shell proteins, MCP, mCP, mC-BP, and SCP, and two precursor internal proteins merge to form a pre-B capsid. The two internal proteins are cleaved developing a B capsid which contain internal scaffolding proteins (Wood et al., 1996). A capsid developed as a result of failed DNA packaging. They contain all of the structural components as a B capsid but lack the assembly protein and are considerably larger than B capsids (Gibson, 1996).
Maturation of HCMV involves the packing of B capsids with viral DNA resulting in the formation of mature C capsids. The C capsid is encompassed of the viral DNA genome and a shell with tegument proteins (Gibson, 1996). In the maturation process, the nuclear lamina is
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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 belongs to the paramyxovirus family of viruses. The virion encompasses a helical nucleocapsid packaged in a lipoprotein envelope attained from the host cell plasma membrane during budding. The external surface of the envelope contains a periphery of surface spikes.
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.
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
HSV is part of the family herpetoviridae and the genus simplexvirus. There are two strains of this virus: HSV1 known as the oral infection and HSV2 known as the genital infection. The structure of the virus is an enveloped, icosahedral capsid, and single linear double-stranded DNA. The capsid contains dsDNA, α and β proteins. The α proteins regulate the reproductive cycle and block the presentation of antigenic peptides on the host membrane. The β proteins are in charge of the viral nucleic acid metabolism and capsid proteins. The glycoprotein spikes are gB, gC, and gD. There are many modes of transmission of the virus like
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
Houghton, M., n.d., Virtual Lab 9: Discovering the Virus Responsible for Hepatitis C, Chiron Corporation, http://www.mhhe.com/biosci/genbio/raven6/lab9/labs/lab9/exp1/index.html, June 28,
Adenoviruses represent the largest non-enveloped or naked viruses at 75 nanometers and have 252 capsomeres that contribute to its icosahedral capsid structure (Doerfler 1996). The virus particle has spikes on the base of each capsomer that aid in attachment to the host cell. At the core of the virus is double-stranded linear DNA that replicates in the nucleus of the host cell.
The main route of transmission of HCV is through large or repeated direct percutaneous exposures to blood (e.g. transfusion or transplantation from infectious donors, injecting drug use) (Lavanchy, 2009).
Herpes simplex virus (HSV) is one of the most prevalent human viral infections worldwide. It belongs to the family Herpesviridae and is composed of linear double-stranded DNA surrounded by icosahedral capsid (Uyangaa et al., 2014). There are two types of herpes virus, namely HSV type 1 and type 2 (HSV-1 and HSV-2), which are the common cause of oral (cold sores) and genital herpes. The HSV infection is highly contagious and can be transferred from person to person through direct close contact. In immunocompromised individuals, HSV infection can lead to even more devastating diseases such as corneal blindness and encephalitis. The HSV is a successful pathogen of humans as, following the primary lesions, it establishes a lifelong latent infection in the sensory neurons (Melchjorsen et al, 2009).
Campbell Eye Microbiology Lab (2016), the standard for HSV laboratory testing is cell culture. Collected samples are layered on a monolayer of cells in test tubes. If present, HSV will present as the cytopathic effect of rounded cells. They use A549 cells as the cell line for testing HSV; this is a human carcinoma continuous cell line. When samples are positive for HSV, the cytopathic effect is present within one to three days. It is rare, but sometimes one to two weeks is necessary to isolate HSV in cell culture. Cell culture will confirm an HSV diagnosis, but it may not provide timely results for immediate patient care. All virology laboratories can offer cell culture isolation of HSV. ELVIS™ (Enzyme Linked Viral Induced System) is another cell culture test, but the results are ready in ONE day. Cells infected with HSV commence a cascade of reactions that results in the accumulation of beta-galactosidase in the cells. Viral samples are layered on the specially engineered cell line in a shell vial and centrifuged. The flask is incubated for one day (overnight), fixed, and stained with a substrate that reacts with the beta-galactosidase. The reactions result in a blue color change in the cells that are observed with an inverted microscope. ELVIS™ testing may also be limited in its availability. PCR is performed for HSV (1 or 2) on specimens collected by soft-tipped applicators, metal spatulas, and jeweler's forceps, and placed in the 2.0ml of chlamydia transport medium. Intraocular fluid or vitrectomy specimen can be supplied directly or increased to a volume of 0.45 ml with chlamydia transport medium. 0.45 ml of the medium is provided for PCR
The hepatitis C virus is a single-stranded RNA virus of the Flaviviridae family. The virus replicates within hepatocytes and is most notable for lacking a proofreading polymerase which enables copious amounts of viral mutations. There are 6 genotypes of HCV with the most widely distributed genotypes being types 1, the most common, and type 2.
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
HEV belongs to genus Hepevirus and family hepeviridae (Acha et al., 2003; International Committee on Taxonomy of Viruses, 2011). HEV differs from hepatitis viruses A, B, C and D both genetically and structurally (Kumar, Das and Jameel, 2010). There are 5 genotypes of HEV. The genotype 1 and 2 viruses are found only in humans, genotype 3 and 4 viruses are found in both human and animals whereas