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      <subfield code="a">Tee, Kok Keng</subfield>
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      <subfield code="a">Thomson, Michael M</subfield>
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      <subfield code="a">Hemelaar, Joris</subfield>
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      <subfield code="a">HIV-1 acquires mutations over time and the virus can also recombine when undergoing replication. Recombination between different HIV-1 subtypes can produce mosaic viral strains which, when causing epidemic spread, are called circulating recombining forms (CRFs). Mutation and recombination lead to genetic diversification onto which evolutionary selection pressures are exerted by effects on the viral replication, transmission, pathogenesis and the immune response. As a result, HIV-1 subtypes have diversified over time and 90 distinct CRFs have been identified globally so far. Phylodynamic and phylogeographic studies estimating the spatiotemporal origin of HIV-1 variants at population level establishes the role of transmission networks in contributing to the rise in new HIV-1 infections. These networks, if left uninterrupted by means of effective intervention strategies, will most likely continue to grow and result in sustained transmission. Understanding the dynamics of growth and dispersal of HIV-1 variants, as well as the cutting edge methods used in such analysis, can be useful to assess the evolution of an epidemic and the impact of public health interventions. However, the epidemiological and molecular mechanisms which contribute to the emergence of recombinants are incompletely understood. Moreover, a better understanding of the effects of HIV-1 genetic diversity on clinical characteristics such as transmission, pathogenesis and disease progression as well as implication for management such as diagnosis, viral load measurement and treatment, are essential for the containment of the HIV epidemic. Finally, the enormous diversity of the HIV-1 pandemic poses a major challenge to the development of a globally effective HIV vaccine.</subfield>
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      <subfield code="a">Tee, K. K., Thomson, M. M., Hemelaar, J., eds. (2022). HIV-1 Genetic Diversity, Volume II. Lausanne: Frontiers Media SA. doi: 10.3389/978-2-88976-940-7</subfield>
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      <subfield code="a">Human Immunodeficiency Virus</subfield>
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