Targeting HIV Replication
The replication of infectious diseases, like HIV 1 is a multi stage process. Each step is crucial for successful replication of infectious diseases, such as HIV and is therefore a potential target for retro viral drugs to try to combat these types of infectious diseases. Step 1 is the infection for the suitable host cell, such as CD4 Positive T lymphocytes. Entry of HIV into the cell, requires a certain presence of certain receptors on the cells surface; CD4 receptors and co-receptors, such as CCR 5 or CXCR4. These receptors combine with protein complexes which are enclosed in the viral envelope. These complexes are composed of 2 glycoproteins, an extra cellular protein, GP120 and a trans membrane GP41.
How HIV Infects A Hosts Cell
Infectious diseases like HIV approaches a target cell and GP120 binds to the CD4 receptors. This is called attachment to bind them together. It promotes further binding to the co-receptor. Co-receptor binding results in the conformation change of the GP120. This allows GP41 to unfold and insert its hydrophobic terminals into the cell membrane. GP41 then turns back on itself. This draws the virus towards the cell and expedites the fusion of their membranes. The viral nucleocapsid enters the hosts cell and breaks open, releasing 2 viral RNA strands and 3 essential replication enzymes: integrase, protease and reverse transcriptase. Reverse transcriptase begins the reverse transciption of the viral RNA. It has 2 catalytic domains, the rival nucleic H active site and the polymerase active site. In this place, single stranded Viral RNA is reproduced into an RNA, DNA double helix. Rival nucleic H breaks down the RNA, the polymerase then completes the remaining DNA strand to form a DNA double helix. Now, integrase goes into action, it cuts a nucleic tide from each 3 prime ends of the DNA, creating 2 sticky ends. Integrase's communication of the DNA into the cell nucleus and promotes its integration into the host cell Genome. The host cell genome now will be comprised of the genetic illumination of HIV. Activation of the cell induces transcription of pro viral DNA into messenger RNA.
The viral messenger RNA migrates into the cytoplasm where building blocks for a new virus are synthesized. A few of them have to be converted by the viral protease. Protease cleaves longer proteins into small core proteins. This step is crucial to create an infectious disease virus. Two viral RNA strands and the replication enzymes then come together and core proteins around them forming the capsid. This immature viral particle leaves the cell gathering a new envelope of host and viral proteins. The virus matures and becomes ready to spread among other cells so infectious diseases like HIV, that are now ready to destroy, can now go to work.
How Antiretroviral Therapy Helps Battle Viral Reproduction
HIV replicates millions of times per day, destroying the host immune cells and eventually causing disease progression. This disease progression can lead to other serious infectious diseases. Drugs, which interfere with the key steps of viral reproduction, can stop this fatal process. Entry into the host cell can be blocked by fusion inhibitors. Inhibition of reverse transcriptase by nucleocide inhibitors or by non nucleaocide non-hibitors, reverse transcriptase inhibitors is part of standard antiviral regimens. The action of integrase can be blocked. Protease inhibitors are also part of standard antiretroviral therapy. Each blocked step in viral replication is a step towards better control of HIV infectious diseases progression.
The replication of infectious diseases, like HIV 1 is a multi stage process. Each step is crucial for successful replication of infectious diseases, such as HIV and is therefore a potential target for retro viral drugs to try to combat these types of infectious diseases. Step 1 is the infection for the suitable host cell, such as CD4 Positive T lymphocytes. Entry of HIV into the cell, requires a certain presence of certain receptors on the cells surface; CD4 receptors and co-receptors, such as CCR 5 or CXCR4. These receptors combine with protein complexes which are enclosed in the viral envelope. These complexes are composed of 2 glycoproteins, an extra cellular protein, GP120 and a trans membrane GP41.
How HIV Infects A Hosts Cell
Infectious diseases like HIV approaches a target cell and GP120 binds to the CD4 receptors. This is called attachment to bind them together. It promotes further binding to the co-receptor. Co-receptor binding results in the conformation change of the GP120. This allows GP41 to unfold and insert its hydrophobic terminals into the cell membrane. GP41 then turns back on itself. This draws the virus towards the cell and expedites the fusion of their membranes. The viral nucleocapsid enters the hosts cell and breaks open, releasing 2 viral RNA strands and 3 essential replication enzymes: integrase, protease and reverse transcriptase. Reverse transcriptase begins the reverse transciption of the viral RNA. It has 2 catalytic domains, the rival nucleic H active site and the polymerase active site. In this place, single stranded Viral RNA is reproduced into an RNA, DNA double helix. Rival nucleic H breaks down the RNA, the polymerase then completes the remaining DNA strand to form a DNA double helix. Now, integrase goes into action, it cuts a nucleic tide from each 3 prime ends of the DNA, creating 2 sticky ends. Integrase's communication of the DNA into the cell nucleus and promotes its integration into the host cell Genome. The host cell genome now will be comprised of the genetic illumination of HIV. Activation of the cell induces transcription of pro viral DNA into messenger RNA.
The viral messenger RNA migrates into the cytoplasm where building blocks for a new virus are synthesized. A few of them have to be converted by the viral protease. Protease cleaves longer proteins into small core proteins. This step is crucial to create an infectious disease virus. Two viral RNA strands and the replication enzymes then come together and core proteins around them forming the capsid. This immature viral particle leaves the cell gathering a new envelope of host and viral proteins. The virus matures and becomes ready to spread among other cells so infectious diseases like HIV, that are now ready to destroy, can now go to work.
How Antiretroviral Therapy Helps Battle Viral Reproduction
HIV replicates millions of times per day, destroying the host immune cells and eventually causing disease progression. This disease progression can lead to other serious infectious diseases. Drugs, which interfere with the key steps of viral reproduction, can stop this fatal process. Entry into the host cell can be blocked by fusion inhibitors. Inhibition of reverse transcriptase by nucleocide inhibitors or by non nucleaocide non-hibitors, reverse transcriptase inhibitors is part of standard antiviral regimens. The action of integrase can be blocked. Protease inhibitors are also part of standard antiretroviral therapy. Each blocked step in viral replication is a step towards better control of HIV infectious diseases progression.
As you can see, HIV is nothing to take lightly and can destroy your immune system rather quickly. Although, anti-retroviral can be useful it will not cure, nor prevent any further antibiotic resistance type problems that can happen. Infectious diseases such as HIV are something that should be left alone. Other relief options that are completely natural may be a better solution.
