How HIV Evades the Body’s Antiviral Responses





How HIV Evades the Body’s Antiviral Responses

Two Canadian molecular virologists, Dr. Eric Cohen, and Mariana Bego have discovered how HIV manages to escape the body’s antiviral responses. In their article, Canadian researchers discover how HIV evades the body’s antiviral responses”, they have given an elaborate explanation as to how HIV is escaping the human body’s response to the virus. This research was done by a group of researchers led by Dr. Cohen, who is a molecular virologist. The study was also done to investigate how the virus has managed to compromise antiviral responses, during the acute infection stage. During this phase, the virus establishes itself in the host and is highly infectious. It was discovered that a HIV viral protein known as VPU tricks the immune system, through its regulatory processes to evade the host’s defenses. The VPU, which stands for Viral Protein Unique, is a protein that degrades the CD4 viral receptor and regulates the CD4 in during a HIV infection. It is often found in the cell membranes of the infected cells (Spearman and Freed 26).

During the acute infection stage, HIV establishes itself in the long-lasting cell reservoirs, which hides the virus from the immune system and the antiviral drugs. This becomes the greatest barrier to finding a cure for HIV. The most important component in this process is the type1 Interferon. Interferons are a group of signaling proteins, which are produced and released by the host cells as a response to invasion by pathogens such as viruses, bacteria, among others. When the body is infected, for instance, with HIV, the cells infected will release interferons, which in turn cause the nearby and surrounding cells to increase antiviral defense, thus the term, signaling proteins (Fensterl and Sen). The greatest challenge is that HIV has now found a way to interfere with the process of the interferon response. Interferons are mostly produced by immune cells called pDCs (plasmacytoid dendritic cells), which are responsible for the defense against pathogenic infections.

Dr. Bego further explains that the production of Interferon is regulated by BST2, a protein that is located on the infected cell’s surface. This happens when the pDCs encounter the HIV-infected cells. BST2 restricts HIV production before it can disseminate through the body. However, it also can activate and bind a receptor called the ILT7, which sends signals that in turn suppress the production of interferons. This strips the interferons off their ability to perform their defensive functions. The ILT7 is found on the pDCs surface. HIV uses the VPU to block and counteract the BST2 antiviral activity. This then allows the virus to multiply and spread throughout the body rapidly. HIV takes advantage of the role that is played by BST2, through activating ILT7, and limiting the production of interferon. The general effect of this is reduced antiviral response, which weakens the immune system.

The findings of this study will provide the scientists with ammunition to improve and enhance antiviral responses and boost the immune system. This will be especially effective during the early stages of infection. Vpu action should be blocked to prevent the virus from expanding and spreading. This will also allow the pDCs to trigger antiviral responses. Such interventions should be carried out during the primary infections stage to limit the complexity of the viral reservoirs, which is important in maintaining a sustained HIV remission. Dr. Cohen observes that the findings of this study have brought scientists and inch closer to finding a cure and ending HIV/AIDS.


Works Cited

Fensterl, Volker, and Ganes C. Sen. ‘Interferons and Viral Infections’. BioFactors 35.1 (2009): 14-20. Web.

Spearman, Paul, and Eric O Freed. HIV Interactions with Host Cell Proteins. Heidelberg: Springer, 2009. Print.

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