Cervical cancer is the third most common type of cancer in women worldwide. A persistent infection with high risk (HR) human papillomavirus (HPV) is necessary for cervical cancer to occur. However, the great majority of women that are infected with HR-HPV will not develop cervical cancer, indicating that HR-HPV alone is not adequate to drive the development of cervical cancer, suggesting the involvement of cofactors. The BK polyomavirus (BKV) establishes latency near cervical tissue in the urogenital tract and is frequently detected in the urine, especially in immunosuppressed patients, and hence may coexist with HR-HPV. Current experimental evidence indicates that both HR-HPV and BKV are capable of altering cell-cycle control and inhibit apoptosis. Therefore, they may act additively or synergistically to promote malignant transformation. We hypothesize that BKV is a co-factor for HR-HPV in cervical cancer. In this study, we examined 249 cervical swabs that were submitted for routine HR-HPV screening test in the Molecular Diagnostics Laboratory at the University of Texas Medical Branch (UTMB). Our results showed that 107 samples contained HR-HPV at an overall rate of 43% (107/249); BKV was present in 4 (3.7%) of the 107 HR-HPV positive specimens and in 12 (8.5%) of the 142 HR-HPV negative samples with an overall positive rate of 6.4% (16/249). Although there was no statistical significance between HR-HPV and BKV co-infection (P=0.19, Fisher's exact test), our results support the hypothesis that BKV can co-exist with HR-HPV in cervical specimens.