Avidin Kft has set up a comprehensive microbial test that can detect all bacteria, fungi and viruses from gynecological samples. The high-sensitivity gynecological microbiome test can simultaneously detect certain subtypes of HPV as well as Chlamydia infections, allowing early detection of high-risk cases described in the study below. Avidin Kft, in cooperation with the Whitelab group, offers to the public this unique method in the market based on sequencing.



It has long been proven that HPV can cause cancer. Indeed, HPV DNA can be found in more than 90% of all cervical cancers. However, HPV is not the sole culprit. Even though more than 80% of women become infected with HPV during their lifetime, not even 2% develop cancer. Cofactors like immune status, hormones, and coinfections are emerging as a causal link in cervical cancer development. Coinfections with Chlamydia trachomatis are seen at an increased incidence in patients with invasive cervical and ovarian cancers, yet the coinfection dynamics and the underlying mechanisms are entirely unknown. Now, scientists at the Max Planck Institute for Infection Biology and the University of Würzburg showed that the collaboration between certain types of viruses and bacteria may lead to cervical cancer.

Their patient-derived, near-physiological, ectocervical, 3D organoid model provides the much-needed in vitro platform to investigate various facets of cervix biology, including the influence on the female reproductive tract and drug testing. This model was used to study infections and coinfections and their molecular mechanisms individual and coinfection dynamics of human papillomavirus (HPV16 E6E7) and Chlamydia trachomatis, published in Nature Communications (https://www.nature.com/articles/s41467-022-28569-1 )

Senior author, Cindrilla Chumduri, Ph.D., chair of Microbiology at the University of Würzburg, added that ”multiple infections create a unique cellular microenvironment that potentially contributes to the reprogramming of tissues and thus to the development of cancer.”

Ectocervical stem cells in the organoids were genetically manipulated to introduce E6E7 oncogenes to mimic HPV16 integration. These organoids developed the characteristics of precancerous lesions, retained self-renewal capacity, and produced mature stratified epithelium similar to healthy organoids. They demonstrated that unique transcriptional and post-translational responses induced by Chlamydia and HPV lead to distinct reprogramming of host cell processes. Several genes were up or downregulated by the two pathogens in different ways, which was associated with specific immune responses. Among other things, Chlamydia impeded HPV-induced mechanisms that maintain cellular and genome integrity, including mismatch repair in the stem cells.

Based on these findings, simultaneous testing of several pathogens bears superior diagnostical values and offers the possibility of treatment of the bacterial infection which may prevent the progression of malignant formation.