V3 loop
The V3 Loop of the Human Immunodeficiency Virus[edit | edit source]
The third variable loop, commonly known as the V3 loop, is a crucial component of the Human Immunodeficiency Virus (HIV). Positioned within the envelope glycoprotein, gp120, of the virus, this loop plays a pivotal role in the virus's ability to invade human immune cells. By facilitating the attachment to specific cytokine receptors on the human immune cell, the V3 loop becomes a critical determinant of HIV's cellular tropism and its pathogenic potential.
Structure and Function[edit | edit source]
The V3 loop's configuration and amino acid sequence are paramount to its functionality. While the overall structure of the gp120 protein aids in the virus's initial binding to CD4 receptors on immune cells, it is the V3 loop that is primarily responsible for the specificity in co-receptor binding[1].
- Binding Specificity: Depending on the strain of HIV, the V3 loop binds to different co-receptors on the human immune cell surface. The two primary co-receptors are:
- CCR5: Many initial HIV infections involve strains that predominantly bind to the CCR5 co-receptor.
- CXCR4: As the infection progresses, some strains might evolve to exploit the CXCR4 co-receptor, which has implications for disease progression and treatment[2].
Clinical Relevance[edit | edit source]
The specificity of the V3 loop in co-receptor binding has significant implications for the course of HIV infection and the therapeutic approaches.
- Tropism Testing: Understanding whether an HIV strain primarily binds to CCR5 or CXCR4 is crucial when deciding on antiretroviral therapy, especially when considering the use of CCR5 antagonists[3].
- Disease Progression: Strains of HIV that utilize the CXCR4 co-receptor are generally associated with faster disease progression and a more aggressive course[4].
Future Research Directions[edit | edit source]
Given the V3 loop's central role in HIV pathogenesis, there is substantial interest in:
- Developing therapies that can inhibit or modify its function.
- Investigating potential vaccines that might target this region of the virus[5].
See Also[edit | edit source]
References[edit | edit source]
- ↑ Moore, J.P., & Doms, R.W. (2003). The entry of entry inhibitors: a fusion of science and medicine. Proceedings of the National Academy of Sciences, 100(19), 10598-10602.
- ↑ Connor, R.I., Sheridan, K.E., Ceradini, D., Choe, S., & Landau, N.R. (1997). Change in coreceptor use correlates with disease progression in HIV-1–infected individuals. The Journal of Experimental Medicine, 185(4), 621-628.
- ↑ Wilkin, T.J., & Gulick, R.M. (2007). CCR5 antagonism in HIV infection: current concepts and future opportunities. Annual review of medicine, 58, 81-93.
- ↑ Koot, M., Keet, I.P., Vos, A.H., de Goede, R.E., Roos, M.T., Coutinho, R.A., ... & Tersmette, M. (1993). Prognostic value of HIV-1 syncytium-inducing phenotype for rate of CD4+ cell depletion and progression to AIDS. Annals of Internal Medicine, 118(9), 681-688.
- ↑ Stanfield, R.L., Gorny, M.K., Zolla-Pazner, S., & Wilson, I.A. (2006). Crystal structures of human immunodeficiency virus type 1 (HIV-1) neutralizing antibody 2219 in complex with three different V3 peptides reveal a new binding mode for HIV-1 cross-reactivity. Journal of virology, 80(12), 6093-6105.
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