Related Experiment Video
Updated: Jul 14, 2026
07:10
Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
Published on: January 7, 2019
Cardiac repolarization is prolonged in CD4C/HIV transgenic mice
Judith Brouillette1, Scott A Grandy, Paul Jolicoeur
1Research Center, Montreal Heart Institute, 5000 Belanger Street, Montreal, Quebec, Canada H1T 1C8.
Journal of Molecular and Cellular Cardiology
|June 29, 2007
Summary
Human immunodeficiency virus (HIV) infection delays cardiac repolarization in mice, independent of medications. This finding suggests HIV itself may cause heart rhythm abnormalities in patients.
Area of Science:
- Cardiology
- Virology
- Molecular Biology
Background:
- Pharmacological treatments for Acquired Immunodeficiency Syndrome (AIDS) can cause QT prolongation and delayed repolarization.
- Emerging evidence indicates delayed repolarization may occur without drug intervention.
- The direct impact of Human Immunodeficiency Virus (HIV) on ventricular repolarization remains uncharacterized.
Purpose of the Study:
- To investigate the effects of HIV on cardiac ventricular repolarization.
- To characterize repolarization changes in a mouse model of HIV disease.
- To determine if HIV infection alone causes delayed repolarization.
Main Methods:
- Utilized CD4C/HIV transgenic mice, which model human AIDS.
- Recorded electrocardiograms (ECG) in conscious mice.
- Employed patch-clamp techniques to analyze action potentials and potassium (K+) currents in ventricular myocytes.
- Conducted echocardiography to assess cardiac structure and function.
Main Results:
- CD4C/HIV mice exhibited significantly prolonged QT intervals and action potential durations compared to wild-type controls.
- A notable reduction in outward K+ currents was observed in HIV transgenic mice.
- Cardiac structure and function remained comparable between HIV transgenic and control mice, ruling out heart failure or hypertrophy as causes.
- Delayed repolarization occurred in the absence of pharmacological agents.
Conclusions:
- HIV infection in mice leads to delayed ventricular repolarization.
- This delay is associated with reduced K+ currents.
- The findings suggest HIV itself, not just its treatment, may be responsible for cardiac repolarization abnormalities.
