While SARS-CoV-2 primarily affects the lungs, the virus may be inflicting detriments to the cardiovascular system, both directly through angiotensin-converting enzyme 2 receptor and initiating systemic inflammation. Persistent systemic inflammation may be provoking vascular dysfunction, an early indication of cardiovascular disease risk. To establish the potential effects of SARS-CoV-2 on the systemic vasculature in the arms and legs, we performed a cross-sectional analysis of young healthy adults (control: 5 M/15 F, 23.0±1.3 y, 167±9 cm, 63.0±7.4 kg) and young adults who, 3–4 wk prior to testing, had tested positive for SARS-CoV-2 (SARS-CoV-2: 4 M/7 F, 20.2±1.1 y, 172±12 cm, 69.5±12.4 kg)(means±SD). Using Doppler ultrasound, brachial artery flow-mediated dilation (FMD) in the arm and single passive limb movement (sPLM) in the leg were assessed as markers of vascular function. Carotid-femoral pulse wave velocity (PWVcf) was asvsessed as a marker of arterial stiffness. FMD was lower in the SARS-CoV-2 group (2.71±1.21%) compared with the control group (8.81±2.96%)(P< 0.01) and when made relative to the shear stimulus (SARS-CoV-2: 0.04±0.02 AU, control: 0.13±0.06 AU, P< 0.01). The femoral artery blood flow response, as evidenced by the area under the curve, from the sPLM was lower in the SARS-CoV-2 group (− 3±91 mL) compared with the control group (118±114 mL)(P< 0.01). PWVcf was higher in the SARS-CoV-2 group (5.83±0.62 m/s) compared with the control group (5.17±0.66 m/s)(P< 0.01). Significantly lower systemic vascular function and higher arterial stiffness are evident weeks after testing positive for SARS-CoV-2 among young adults compared with controls.