The has been two major breakthroughs that have brightened the hope of an effective vaccine against the Human Immunodeficiency Virus {HIV} and Acquired Immune Deficiency Syndrome {AIDS}. First is the discovery of how HIV evades the human body's immune system. The second is the identification of cellular proteins recruited by HIV to compromise CD4+T cell {essential immune cells} function and enhance viral replication.
The more in-depth understanding of the ways in which HIV mutates to avoid the human immune system will help with the design of an HIV vaccine and new class of drugs to combat it. Though HIV type 1 {HIV-1} causes AIDS by depleting essential immune cells called CD4+T lymphocytes in infected individuals, resulting in a compromised immune system. "At the centre of this process is the HIV protein, viral protein R {Vpr}, which stops infected CD4+T cells from dividing and as a consequence compromises their immune function. In addition, by arresting cell division, Vpr helps HIV to harness the infected cell's resources to enhance viral replication.
The way Vpr exerts this effect is by interacting with cellular proteins that control cell division". The first breakthrough is a pioneer methods to how the HIV mutates escape the body's immune system. A controlling part of the human immune response - can influence HIV genetic sequence, as well as the first characterization of changes in multiple HIV genes in response to HLA-associated evolutionary pressure. The second is a novel cellular protein complex targeted by HIV-1 Vpr to stop infected cell from dividing. This protein complex, designated DDB1-CUL4-VprBP, is involved in a process called ubiquitination.
Ubiquitination is a mechanism by which a small protein called ubiquitin is conjugated to cellular proteins in order to modulate their biological activity or induce their degradation. The Vpr with this ubiquitinating complex, also called an E3 ubiquitin ligase complex, is essential for the defect in cell division induced by Vpr. Further characterisation of this protein complex as well as the elucidation of the mechanism by which it affects cell division may open new avenues for therapeutic intervention against HIV. Meanwhile, "Achieving a more in-depth understanding of the ways in which HIV mutates to avoid the human immune system will help with the design of an HIV vaccine." Indeed, the ability of HIV to escape recognition by HLA class 1 leaves the body incapable of finding and fighting the virus. particulary HIV genes with variations can improve the virus' ability to escape immune recognition, showing this is predictable based upon the HIV patient's on individual HLA class 1 profile.
"This is a novel and advanced description of how the human immune system attacks the virus, and how it responds. While the body attacks the virus and the virus changes to dodge pressure.
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