Viruses are obligate intracellular parasites; their lack of biochemical machinery makes them dependent on the host cell for replication.5,8 The viral replication process involves assembly individual components into viral progeny. Viruses consist of a DNA or RNA genome that is packaged into a protective protein capsid shell; additionally, some viruses are surrounded by an outer, membranous envelope.2,5,8 Viral genomes are used to express viral proteins.5 However, because these viral genomes do not encode for the machinery necessary to carry out protein synthesis, viral genomes must be copied into mRNA that can be read by host ribosomes.5,7,8 There are seven major types of viral genomes that are classified by the Baltimore system. 5 All viruses …show more content…
1,5,7 Alphaherpesvirus virion fuses its envelope with the host cell plasma membrane, releasing the nucleocapsid into the cytoplasm; the nucleocapsid then associates with the nuclear membrane, delivering the genome into the nucleus where the dsDNA genome is transcribed and replicated. 1,5-8 Unlike paramyxoviruses whose genome cannot be directly translated, the alphaherpesvirus genome is directly transcribed into mRNA by host cell DNA-dependent RNA polymerase in the host nucleus. The mRNA is then translated on host ribosomes to synthesize viral proteins. Genome replication and gene expression occurs in three stages:
1. Immediate early proteins are expressed first. These proteins are required for co-opting the host cell biochemical machinery and regulating transcription.
2. Early proteins are expressed next. A viral-encoded DNA-dependent DNA polymerase is expressed and is used to produce viral dsDNA
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4,5 The DNA intermediate is integrated into the host chromosome to become a cellular gene. 4,5 This DNA an also serves as a template for viral mRNA and genome RNA synthesis by host cell DNA-dependent RNA polymerase. 4,5,7,8 The retroviral genome consists of three genes that encode polyproteins for Gag (capsid, matrix and nucleic acid binding proteins), Pol (polymerase, protease and integrase) and Env (envelope proteins).
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.
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.
Step 1: How will you identify the “vital” cellular protein that the virus targets for degradation? (Hint: think proteomics). (3 pts.)
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
Transcription occurs in the nucleus involving what is known as "cap snatching." What this means is that the viral endonuclease (PB2) cuts the 5' methylguanosine cap as well as ten to thirteen nucleotides from the RNA. This is then used as the primer for the transcription of the protein PB1, a viral transcriptase. In influenza A and B, ten proteins result from the translation of the eight segments of the genome, including hemagglutinin,
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.
The HIV-1 life cycle is complicated and its period and result is contingent upon the target cell type and cell activation. In the beginning, HIV-1 enters the cells without producing instant damage but by entering the cells it can provoke intracellular signal cascades, which may assist the progress of viral replication. The external glycoprotein (gp120) and the transmembrane protein (gp141) are two molecules on the HIV-1 envelope that form the spikes on the virion’s surface. In the entry process, gp120 first attaches to the CD4+ receptor and then attaches to the cell membrane. Interactions between the virus and chemokine co-receptors will cause permanent conformational changes. The fusion event will occur within minutes by pore formation and it will discharge the viral core into the cell cytoplasm. Once the core dismantles, the viral genome will be reverse transcribed into DNA by the virus’ own reverse transcriptase enzyme. Viral variants may develop at the time of this process because reverse transcriptase is error prone. During the midpoint of infection, both the viral protein integrase and the host DNA repair enzymes will inject the viral genome into the active domain of the host’s chromosomal DNA. Lens epithelium-derived growth factor (LEDGF/p75) is an integrase binding host factor that assists the progress of integration, which converts the cell into a virus producer. In the late stages, production of viral particles will need both host driven and virus driven
This little package of mayhem consists of relatively few parts. A virus is simply a protein capsule called a capsid, sometimes surrounded by an envelope, containing a genome. The genome consists of nucleic acids arranged as DNA or less commonly, RNA. Dozens of variants of this fundamental arrangement exist with differences in the structure of the capsule and the arrangement of the genome. Small differences or changes in these components allow some viruses to continue to outmaneuver researchers, while millions of dollars are spent trying to understand and eliminate them.
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
Once the virus has entered a host cell, the virus releases the RNA strand to be replicated and form more viruses until
The juxtapositional co-receptor attachment to the host membrane encourages the GP41 protein to initiate fusion by collapsing into a hairpin loop structure bringing the two membranes in close proximity. The virus then injects the contents of the virion including machinery enzymes and the RNA genome into the host cell where a dsDNA molecule is made and integrated into the host. The reverse transcription process has a high mutation rate because the viral reverse transcriptase enzyme is unable to detect or repair any mistakes as it forms the dsDNA. After the new dsDNA molecule is made it is transported to the nucleus of the host and integrated into the host genome. The HIV genome will either remain in a lysogenic state within the host or if actively stimulated new HIV viruses will be constructed and released to infect neighboring cells.
Hepatitis B is an enveloped bacterium, meaning that it has an outer coding that protects it from the host cell. As mention earier in the above paragraph, these viruses genetic materials are made up of DNA. It has spikes on the outside and the core proteins surrounding the chromoses on the inside of them. The spikes are attach to a lipid bilayer membrane. For instead in the case of transcription and translation the virus does not need to translate the viral DNA into RNA to make copies of the virus, because the virus itself is already in a DNA form. DNA-to-DNA translation between the host and the viral chromosomes takes place very easily. Most RNA viruses required core enzymes to help translate the viral RNA into DNA, this then assist the viral DNA to match with the host DNA and then after it turns right back into an RNA. Since these viruses are in the DNA form, I will say they don’t required core enezymes to replicate; so they donot have core enyemes. This viral DNA is part stranded. It use the host eneymes to get the job done,
These are the endogenous viruses and some individuals can have thousands of copies of these A-type viruses in their chromosomal DNA. B-type viruses have an eccentric core and the mammary tumor viruses exclusively possess this structure (Cloyd, M) . These viruses exist as endogenous and exogenous viruses and when expressed can cause mammary tumors. C-type viruses have a central electron core (Cloyd, M) . Most of the oncoviruses and endogenous viruses are C-type viruses. The D-type viruses have a rod-shaped core and consist primarily of lentiviruses (Cloyd, M) . HERVs are a subclass of a gene known as transposon. These genes can be packed and moved within the genome to serve a vital role in gene expression and regulation. HERVs have been grouped into three broad classes, based on the sequence similarities, which are broken into subgroups based on the specificity of their tRNA binding site. Class I HERVs are related to gamma retroviruses such as murine leukemia viruses (Griffiths, D). Class I includes the subgroups of HERV-W and HERV-H. Class II HERVs are related to beta retroviruses such as mammary tumor viruses and include several subtypes of HERV-K elements (Griffiths, D) . Class III HERVs are related to spumaretrovirueses and subgroups include HERV-L and HERV-S (Griffiths, D) . Class I and class III are the oldest groups, seen in primitive lineage, and class II includes those active most recently. HERVs
Once the viral dsDNA has entered the nucleus, if it circularizes itself and becomes an episome within the nucleus, then the virus has entered a lytic life cycle. EBV replication takes place in specialized sites within the host nucleus, referred to as replication compartments8. It is believed that EBV replicates following the rolling circle replication model1. Figure 3 demonstrates how RCR works: after being cut with an endonuclease one strand is replicated continuously and the other is replicated discontinuously, putting together segments called linear concatamers and they code for circular DNA. Once EBV replication has begun the three stages of transcription begin to follow.
Viruses are obligate intracellular parasites, which means that they cannot grow outside the host cell, they always require a host cell for their multiplication. They use the host machinery for its multiplication. They can