Related Experiment Video
Updated: Aug 1, 2026

07:10
Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
Published on: January 7, 2019
15.8K
Evolution of SIVmac239 following serial passaging in humanized mice
James Z Curlin1,2, Kimberly Schmitt1, Leila Remling-Mulder1
1Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA.
Journal of Medical Primatology
|August 28, 2022
Summary
Serial passage of simian immunodeficiency virus (SIVmac239) in humanized mice reveals ongoing adaptive mutations. This process leads to persistent CD4+ T cell loss and increased viral loads, offering insights into lentivirus cross-species transmission.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Primate lentiviruses, like SIVmac239, can transmit across species.
- Understanding the genetic adaptations required for human transmission is crucial for preventing zoonotic diseases.
Purpose of the Study:
- To investigate the adaptive genetic changes in SIVmac239 during serial passage in humanized mice.
- To assess the impact of these adaptations on host immune response and viral replication.
Main Methods:
- Serial passage of SIVmac239 in humanized mouse models.
- Monitoring of CD4+ T cell counts and plasma viral loads.
- Analysis of accumulating adaptive mutations in the viral genome.
Main Results:
- Four serial passages of SIVmac239 resulted in continued accumulation of adaptive mutations.
- Persistent decline in CD4+ T cell populations was observed throughout the passages.
- Significant increases in plasma viral loads were detected.
Conclusions:
- Serial passage drives adaptive evolution of SIVmac239 in a humanized host.
- These adaptations correlate with immune pathogenesis, including CD4+ T cell depletion.
- Findings provide a model for studying lentivirus adaptation and cross-species transmission potential.

