The Testes Are Highly Microvascularized: Acute COVID Can Damage the Testes, Long COVID-Spike Exposure May Slowly Damage Them Reducing Male Fertility

Key Takeaways

• Acute COVID can cause testicular microvascular damage, impairing sperm production
• Study of 875 men shows ultrasonic microvascular density predicts micro‑TESE success
• Spike protein detected in testicular arteries of a patient with infarction
• Combined UMVD >28.5/cm² and UVE >8.94 mL yields 79% sensitivity for sperm retrieval
• Researchers urge large‑scale studies on viral antigen persistence and vascular health

Pulse Analysis

The global fertility rate has slipped from 5 children per woman in 1950 to just above the replacement level today, prompting concerns across health agencies. While lifestyle and environmental factors have long been blamed, emerging evidence points to SARS‑CoV‑2 as a biological stressor that can directly impair male reproductive capacity. The testes are among the most densely microvascularized organs, making them vulnerable to viral‑induced endothelial injury. Acute COVID‑19 episodes have been linked to orchitis, testicular infarction and reduced sperm parameters, suggesting a plausible pathway from infection to lower fertility.

A 2024 ultrasound study of 875 men quantified this vulnerability by measuring ultrasonic microvascular density (UMVD) and testicular volume (UVE). Participants with successful micro‑dissection testicular sperm extraction (micro‑TESE) displayed UMVD above 28.5 cm⁻² and UVE over 8.94 mL, achieving a combined diagnostic accuracy of 86 % (AUC 0.856). These metrics provide clinicians with a non‑invasive predictor of sperm retrieval outcomes, potentially sparing patients from unnecessary surgery. The findings also reinforce the hypothesis that microvascular loss—whether from infection, inflammation or comorbidities—can be a hidden driver of male infertility.

Beyond individual cases, the broader public‑health picture remains uncertain. Isolated pathology, such as the reported spike‑protein‑positive obliterative arteritis leading to testicular necrosis, raises questions about long‑term antigen persistence after infection or vaccination. Large‑scale, population‑based studies that stratify participants by COVID‑19 exposure, vaccination status and vascular health are essential to quantify any chronic fertility risk. If a causal link is confirmed, reproductive‑health screening could become a routine component of post‑COVID care, and therapeutic strategies targeting endothelial repair might mitigate the hidden cost of the pandemic on the next generation.