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Abstract

Human immunodeficiency virus (HIV) is a retrovirus that is classified in the genus Lentivirus. Lentiviruses are uniquely distinguished from other retroviruses by having a long latency period between infection and the manifestation of symptoms, a characteristic that confers the genus its Latin etymology (lentus being the adjective for “slow”) [1]. Moreover, lentiviruses are transmitted between hosts without the need for an intermediate vector, infect a broad range of mammalian hosts, and have a worldwide distribution. There are presently seven recognized major lentivirus lineages reflecting the known mammalian host range (lagomorph, equine, small ruminant, bovine, feline, prosimian, and simian [2, 3]). The virus genomes representing these lineages share a common genomic structure comprising three major genes (gag, pol, and env) and two regulatory genes (tat and rev); however, there are also a number of accessory genes that vary in number, type and relative location (Fig. 23.1).

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Notes

  1. 1.

    At the production stage of this book chapter, a paper from D’arc et al. was published online in the Proceedings of the National Academy of Sciences (USA) presenting new evidence that HIV-1 group O was most likely introduced into the human population from gorillas (SIVgor) which in turn derived from SIV in chimpanzees (SIVcpz).

  2. 2.

    A molecular phylogeny is a tree that represents how genetic sequences are related by common ancestors.

  3. 3.

    Note that we do not assume that synonymous mutations evolve neutrally in an absolute sense; they are only being used as a frame of reference to measure the evolutionary consequences of changes in the amino acid sequence. Without a doubt, selection operates on the HIV genome at the level of the nucleotide sequence. For example, the HIV RNA genome folds into a complex and functionally significant secondary structure due to Watson-Crick base pairing interactions [71].

  4. 4.

    In the original frequentist framework, the nonsynonymous and synonymous rates are usually denoted by d N and d S , respectively. By convention, selection is measured by the ratio ω = d N /d S , such that the null hypothesis of neutral protein evolution is represented by ω = 1. One drawback of using this ratio is that it becomes numerically unstable when the number of synonymous substitutions is low. More generally, the ratio of two random variables has problematic statistical properties which can lead to severe biases under some conditions [92].

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Joy, J.B., Liang, R.H., Nguyen, T., McCloskey, R.M., Poon, A.F.Y. (2015). Origin and Evolution of Human Immunodeficiency Viruses. In: Shapshak, P., Sinnott, J., Somboonwit, C., Kuhn, J. (eds) Global Virology I - Identifying and Investigating Viral Diseases. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-2410-3_23

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