
ASSOCIATION OF RELATIVE TELOMERE LENGTH
AND RISK OF HIGH HUMAN PAPILLOMAVIRUS LOAD
IN CERVICAL EPITHELIAL CELLS Albosale A H, Mashkina E V *Corresponding Author: Dr. Abbas Hadi Albosale, Genetics Department, Southern Federal University,
344090, Stachki, 194/1, Rostov-on-Don Province, Russia. E-mail: abbashammadi4@gmail.com page: 65
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DISCUSSION
Persistent high-risk human papillomavirus infection
is the primary cause of cervical malignant neoplasm lesions
[26]. As viral loads increase, in response to protracted
exposure, the risk of epithelial cell dysplasia also increases.
Thus, there is a discernible correlation between elevated
viral loads and the incidence of abnormal lesions and cervical
malignant neoplasms [27].
In the current study, cell samples taken from 50 participants
with high HPV loads were investigated to ascertain
whether telomere length could be employed as a potential
diagnostic tool for women who are high-risk HPV positive.
Thus, this study has enabled a comparative analysis of the
relative telomere lengths in the DNA samples from cervical
cell samples taken from participants with high HPV loads
with those taken from participants in a control group. No
significant differences were reported between participants
with HPV loads of 4-5lg and those with HPV loads of
>5lg. However, in both HPV load groups, the telomeres
were shorter than what was observed in the control group.
Thus, telomere shortening could be an initial molecular
modification in advance of the development of high-risk
HPV carcinogenesis [28]. The results emerging from the
current study indicate that telemetric DNA undergoes shortening
in cervical cell samples where the HPV load exceeds
4 lg. Early cervical tumorigenesis is characterized by either
telomere dysfunction (the loss of telomere capping function)
or excessive telomere erosion, both of which generate
chromosomal aberrations that lead to oncogenesis [29].
Studies indicate that there is a link between substantially
shortening telomeres and both the activation of the
DNA damage response pathway (Chk2 phosphorylation)
and an increase in cervical cell proliferation [30]. Shortened
telomere length is associated with complex, nonreciprocal
chromosomal translocations, genome amplification,
deletion via breakage–fusion–bridge (BFB) cycles,
and the development of epithelial carcinomas and other
malignancies [31,32].
Marginal increases or predispositions to increase have
been observed in association with viral loads that exceed
5 lg. The viral loads represent the number of infected cells
and viral copies in individual cells. Thus, increased viral
loads are linked to increased incidences of cervical cancer.
Studies have shown that there is a rise in telomerase
activity that corresponds with lesion development, ranging
from low-grade squamous intraepithelial lesions (LSIL) to high-grade squamous intraepithelial lesions (HSIL),
and onwards to invasive cervical cancer. This indicates
that telomere length abnormalities constitute a common
genetic change that transpires during the many stages in
the development of malignant transformation. This correlates
with dysplasia and telomerase activity. Furthermore,
it increases with the progression of lesions [20,33–37].
There are several limitations to the current research
project, the first of which is that the sample included no
participants with either cervical cancer or histological lesions.
This rendered it impossible to examine telomere
alterations in lesions that were at a more advanced stage.
The second major limitation pertains to the comparatively
small size of the study sample, which might preclude generalization.
It is necessary, therefore, to confirm the findings
of this study in a larger population.
In conclusion, the current study has revealed that
shortened telomeres are present in cervical samples taken
from participants who are HR-HPV positive and have
elevated viral loads. Thus, telomere length has a potential
application in future triaging, monitoring, and screening of
women with high-risk HPV infections. It must be reiterated,
however, that additional research with a larger sample
group is needed before this hypothesis can be confirmed.
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