HCV, or the hepatitis C virus, has one primary goal after it has initially infected a new host. This virus must seek out and attach itself to the cells of the liver. Once the virus has effectively been able infect the liver cells, it can start to reproduce. This in a nutshell is the entire lifecycle of the virus, and exactly why it is associated with liver disease. Medical researchers still have much to learn about this virus, but just like many other viruses, there are eight key steps which are essential to completing its life cycle. If you live in Florida and have Hep C, you may want to check out Avail's Hepatitis C Clinical Trials.
Step 1: Locating Liver Cells to Infect
This step is pretty straight forward. Hepatitis C has one goal in mind after entering the body, finding some healthy liver cells. Unfortunately, this virus is particularly well equipped for the task. Located on its protective lipid coat are these certain proteins which the virus uses to attach itself to the receptor site of the liver cell.
Step 2: The Virus Enters the Cell
Frankly, this whole process is very similar to a hostile takeover. The hepatitis C virus uses its protein core to penetrate the plasma membrane of the liver cell. The virus is able to accomplish this forceful entry by merging its lipid coat with the outer membrane of the liver cell. You may be wondering exactly how this is possible. Incredibly, the protective lipid coat of the HCV is actually made up of some fragments from the plasma membrane of another liver cell! Once this fusion of lipid coat and plasma membrane has been successfully made, the entire virus is engulfed by the membrane. Now that the core of the hepatitis C virus is inside the cell, some real damage can begin.
Step 3: Release of the HCV RNA
Once inside the cell, the HCV's protein coat dissolves and its RNA is released into the cell. The protein coat can be dissolved in two different ways. Most often it dissolves when the hepatitis C penetrates the cell membrane; the protein coat actually breaks open when it enters the cells cytoplasm. Sometimes, there are special enzymes present in the liver cell which can be used to dissolve the protein.
Step 4: Appropriation of the Liver Cell's Ribosomes
Now the HCV's RNA can actually take control of the cell's ribosomes. Once it has control, it forces the cell to produce the necessary materials that it needs to reproduce. This whole process is possible, because the hepatitis C virus is able to store all of its information on the strand of RNA. The liver cell's ribosomes are able to read this RNA directly, pretty much acting the same as the mRNA already present in the cell. Once production of these necessary materials begins, the virus often shuts down most of the normal functions of the cell. This way, the virus is effectively forcing the cell to conserve vital energy for the production of more viral material. However, some hepatitis C clinical studies have shown that this virus may stimulate the cell to reproduce itself. It is assumed that this way there will be more cells which can produce even more viral material. This happens to be the reason that hepatitis C is often linked to liver cancer.
Step 5: Creation of Antisense Version
Once the viral RNA has effectively synthesized the amount of RNA transcriptase that it needs for reproduction, the HCV RNA can then produce an antisense version of itself. Basically, an antisense version is the exact opposite copy which will be used as a template of sorts in order to create brand new viral RNA. This new RNA is then copied over and over thousands of times, producing the genetic material for new viruses. Hepatitis research has shown that some of this new RNA will contain mutations.
Step 6: Capsomeres
Now the hepatitis C RNA can start the production of the protein based capsomeres, which will serve as the building blocks for the HCV's protective protein coat. The liver cells ribosomes will create these proteins and then release them for use.
Step 7: Formation of the Nucleocapsid
The brand new capsomeres begin to assemble themselves around the new viral RNA, creating new viral particles. These capsomeres are designed in a certain way so that they are attracted to each other and fit together in a certain way. Once enough of these capsomeres have been brought together, they will form a perfectly spherical shell, which is called a capsid. This capsid fully encloses the new HCV RNA, and the completed particle is known as a nucleocapsid.
Final Step: Release of the New Viruses!!
Once these new hepatitis C viruses have been properly formed, they will attach themselves to the inside portion of the plasma membrane. This formation is known as a bud. Once this has occurred, the cells plasma membrane will encircle the virus. This whole process not only allows the new virus to be released from the cell, but it also provides the new HCV with its vital protective lipid coat. This whole process of budding and releasing of new HCV viruses continues for hours, until the liver cell eventually dies from overexertion.
The Unfortunate Conclusion
Unfortunately, every single one of these new hepatitis C viruses has the ability to produce thousands of more €offspring€. Now, many of these viruses will be destroyed by the body's immune system and even some other environmental factors, but this cycle of reproduction does not stop. In the long-run, it will cause significant damage to the liver, as more and more cells are destroyed on a larger and larger scale.
Step 1: Locating Liver Cells to Infect
This step is pretty straight forward. Hepatitis C has one goal in mind after entering the body, finding some healthy liver cells. Unfortunately, this virus is particularly well equipped for the task. Located on its protective lipid coat are these certain proteins which the virus uses to attach itself to the receptor site of the liver cell.
Step 2: The Virus Enters the Cell
Frankly, this whole process is very similar to a hostile takeover. The hepatitis C virus uses its protein core to penetrate the plasma membrane of the liver cell. The virus is able to accomplish this forceful entry by merging its lipid coat with the outer membrane of the liver cell. You may be wondering exactly how this is possible. Incredibly, the protective lipid coat of the HCV is actually made up of some fragments from the plasma membrane of another liver cell! Once this fusion of lipid coat and plasma membrane has been successfully made, the entire virus is engulfed by the membrane. Now that the core of the hepatitis C virus is inside the cell, some real damage can begin.
Step 3: Release of the HCV RNA
Once inside the cell, the HCV's protein coat dissolves and its RNA is released into the cell. The protein coat can be dissolved in two different ways. Most often it dissolves when the hepatitis C penetrates the cell membrane; the protein coat actually breaks open when it enters the cells cytoplasm. Sometimes, there are special enzymes present in the liver cell which can be used to dissolve the protein.
Step 4: Appropriation of the Liver Cell's Ribosomes
Now the HCV's RNA can actually take control of the cell's ribosomes. Once it has control, it forces the cell to produce the necessary materials that it needs to reproduce. This whole process is possible, because the hepatitis C virus is able to store all of its information on the strand of RNA. The liver cell's ribosomes are able to read this RNA directly, pretty much acting the same as the mRNA already present in the cell. Once production of these necessary materials begins, the virus often shuts down most of the normal functions of the cell. This way, the virus is effectively forcing the cell to conserve vital energy for the production of more viral material. However, some hepatitis C clinical studies have shown that this virus may stimulate the cell to reproduce itself. It is assumed that this way there will be more cells which can produce even more viral material. This happens to be the reason that hepatitis C is often linked to liver cancer.
Step 5: Creation of Antisense Version
Once the viral RNA has effectively synthesized the amount of RNA transcriptase that it needs for reproduction, the HCV RNA can then produce an antisense version of itself. Basically, an antisense version is the exact opposite copy which will be used as a template of sorts in order to create brand new viral RNA. This new RNA is then copied over and over thousands of times, producing the genetic material for new viruses. Hepatitis research has shown that some of this new RNA will contain mutations.
Step 6: Capsomeres
Now the hepatitis C RNA can start the production of the protein based capsomeres, which will serve as the building blocks for the HCV's protective protein coat. The liver cells ribosomes will create these proteins and then release them for use.
Step 7: Formation of the Nucleocapsid
The brand new capsomeres begin to assemble themselves around the new viral RNA, creating new viral particles. These capsomeres are designed in a certain way so that they are attracted to each other and fit together in a certain way. Once enough of these capsomeres have been brought together, they will form a perfectly spherical shell, which is called a capsid. This capsid fully encloses the new HCV RNA, and the completed particle is known as a nucleocapsid.
Final Step: Release of the New Viruses!!
Once these new hepatitis C viruses have been properly formed, they will attach themselves to the inside portion of the plasma membrane. This formation is known as a bud. Once this has occurred, the cells plasma membrane will encircle the virus. This whole process not only allows the new virus to be released from the cell, but it also provides the new HCV with its vital protective lipid coat. This whole process of budding and releasing of new HCV viruses continues for hours, until the liver cell eventually dies from overexertion.
The Unfortunate Conclusion
Unfortunately, every single one of these new hepatitis C viruses has the ability to produce thousands of more €offspring€. Now, many of these viruses will be destroyed by the body's immune system and even some other environmental factors, but this cycle of reproduction does not stop. In the long-run, it will cause significant damage to the liver, as more and more cells are destroyed on a larger and larger scale.
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