In 2010, we reported VTE in multiple organs of a patient who died of SARS, suggesting viral infection is a cause of systemic VTE (9) . In addition, in 2010, we detected virus-like microorganisms in the lymphocytes of a young pulmonary hypertension patient with increased D-Dimer, which morphologically confirmed the attack of T cells by virus, and peripheral decreased CD3 + and CD8 + level also indicated virus infection caused significantly compromised function of T cells (10) . In 2011, we reported the decreased CD3 + and CD8 + level with an increased CD4 + /CD8 + ratio in a group of CTEPH patients, suggesting T cellular immune dysfunction and ratio imbalance in CTEPH patients (11) . In the present study, the whole human genome microarray and Gene Ontology (GO) analysis were employed to detect the targeting of symptomatic pulmonary embolism (PE). In addition, flow cytometry was performed to investigate the changes in immune cells in VTE patients, which aimed to validate the results from genome analysis. Based on the findings above, the relationship between immune dysfunction and clinical symptomatic VTE was analyzed. The CPR level in part of VTE inpatients was determined.