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HIV‐1 emerged from SIVcpz evolving in humans. Humanized mice are an effective tool for assessing viral evolution via measuring viral loads, CD4+ T cell decline, and analyzing genetic changes. Four serial passages showed many non‐synonymous mutations important for the adaptation and evolution of SIVcpz to human immune cells. [ABSTRACT FROM AUTHOR]

HIV‐2 Group F virus with an origin in NHPs was isolated from only two individuals. Two serial passages in hu‐mice showed increased viral loads, CD4+ T cell decline and nonsynonymous genetic changes showing its capacity for further evolution, and spread in the human. [ABSTRACT FROM AUTHOR]

Critical genetic adaptations needed for SIV chimpanzee to evolve into HIV‐1 are not well understood. Using humanized mice, we mimicked the evolution of SIVcpzLB715 into HIV‐1 Group M over the course of four generations. Higher initial viral load, increased CD4+ T‐cell decline, and nonsynonymous substitutions arose suggesting viral evolution. [ABSTRACT FROM AUTHOR]

Serial passage of SIVmac239 allows for greater understanding of the genetic changes necessary for cross‐species transmission of primate lentiviruses into humans. Using humanized mice, we show that adaptive mutations continue to accumulate in SIVmac239 during four serial passages, with persistent CD4+ T cell decline and increases in plasma viral loads. [ABSTRACT FROM AUTHOR]

Through the accumulation of adaptive mutations, HIV‐2 originated from SIVsm. To identify these evolutionary changes, a humanized mouse model recapitulated the process that likely enabled this cross‐species transmission event. Various adaptive mutations arose, as well as increased virulence and CD4+ T‐cell decline as the virus was passaged in humanized mice. [ABSTRACT FROM AUTHOR]

HIV‐1 evolved from SIV during cross‐species transmission events, though viral genetic changes are not well understood. Here, we studied the evolution of SIVcpzLB715 into HIV‐1 Group M using humanized mice. High viral loads, rapid CD4+ T‐cell decline, and non‐synonymous substitutions were identified throughout the viral genome suggesting viral adaptation. [ABSTRACT FROM AUTHOR]

HIV‐1 evolved from its progenitor SIV strains, but details are lacking on its adaptation to the human host. We followed the evolution of SIVcpz in humanized mice to mimic cross‐species transmission. Increasing viral loads, CD4+ T‐cell decline, and non‐synonymous mutations were seen in the entire genome reflecting viral adaptation. [ABSTRACT FROM AUTHOR]

Abstract: How SIV progenitors evolved into deadly HIV‐1 and HIV‐2 following initial cross‐species transmission still remains a mystery. Here, we used humanized mice as a human surrogate system to evaluate SIVsm evolution into HIV‐2. Increased viral virulence to human CD4+ T cells and adaptive genetic changes were observed during serial passages. [ABSTRACT FROM AUTHOR]