Abstract
Human immunodeficiency virus (HIV) is an extraordinarily variable virus. This is in part a result of a lack of a proofreading mechanism and the consequential high error rate, a feature shared by all RNA viruses (0.2–2 mutations per genome per cycle) (1), a high replication rate, as well as an apparent high tolerance and selection for change. As a result of this variability, HIV is a particularly formidable opponent for those who seek ways to counter it. While any given HIV infection generally starts out with a relatively homogeneous virus population (2), over the course of the infection viruses that have mutated to alter more than 10% of their genetic information can arise (3–6). The variants that emerge in an individual (together considered a quasispecies) can differ in biological properties such as drug sensitivity (7–9), coreceptor specificity (10–12), and immunological susceptibility (13–15). The viral quasispecies in a single individual is capable of eluding virtually any antiviral medication given as monotherapy (but not combination therapy 16), and of slipping past the host’s immune response.
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Korber, B.T., Foley, B., Gaschen, B., Kuiken, C. (2001). Epidemiological and Immunological Implications of the Global Variability of HIV-1. In: Pantaleo, G., Walker, B.D. (eds) Retroviral Immunology. Infectious Disease. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-110-7_1
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