Background: As a part of our search for oncogenic
viruses as potential etiological agents in human malignancies,
our studies on human papillomaviruses (HPV) were extended
to analysis of the 3 polyomaviruses (SV40, BKV and JCV) in
colorectal carcinomas. Patients and Methods: Archival tumour
samples from 71 patients with colorectal cancer were analyzed
for the sequences of SV40, BKV, JCV and HPV using PCRbased
techniques. HPV genotypes were determined using
sequencing and reverse blot hybridization (InnoLipa). Results:
Amplification of BKV and JCV with the primer pair PEP-1
and PEP-2 and subsequent restriction digestion of the
amplified products with BamH I disclosed BKV in 6/66 (9%)
of the samples, whereas none contained JCV. SV40 was
amplified in 10/66 (15.1%) samples and confirmed by
sequencing analysis. In pair-wise analysis for co-infections, the
samples were significantly different in their BKV-JCV and JCVSV40
status, in contrast to their BKV-SV40 co-infection status.
HPV DNA was detected in 22/66 (33.3%) of the samples
analysed with either the MY09/11 or SPF primer mix. Of these
22 HPV infections, 7 were single-type infections and 15
contained multiple HPV types. HPV detection or type
distribution showed no relationship to the gender of the
patients or histological grade of the tumour. HPV status was
not significantly related to detection of BKV, JCV or SV40.
Similarly, in pair-wise analysis for co-infections, the samples
were significantly different in their status of HPV-BKV
(p=0.0006), HPV-JCV (p=0.0001), and HPV-SV40
(p=0.019), implicating that HPV and the 3 polyomaviruses are
rarely detected concomitantly in the same samples.
Conclusion: Taking the known molecular mechanisms of
action of these individual viruses, there is a chance that these
viruses could alter the mechanisms of cell cycle control and
inhibit apoptosis, thus potentially causing chromosomal
instability and promoting colorectal oncogenesis.
