The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual's susceptibility to cervical disease.

One of the most widely used types of assisted reproduction technology is the in vitro fertilization (IVF), in which women undergo controlled ovarian stimulation through the administration of the appropriate hormones to produce as many mature follicles, as possible. The most common hormone combination is the co-administration of gonadotropin-releasing hormone (GnRH) analogues with recombinant or urinary-derived follicle-stimulating hormone (FSH). In the last few years, scientists have begun to explore the effect that different gonadotropin preparations have on granulosa cells’ maturation and apoptosis, aiming to identify new predictive markers of oocyte quality and successful fertilization. Two major pathways that control the ovarian development, as well as the oocyte–granulosa cell communication and the follicular growth, are the PI3K/Akt/mTOR and the Hippo signaling. The purpose of this article is to briefly review the current knowledge about the effects that the different gonadotropins, used for ovulation induction, may exert in the biology of granulosa cells, focusing on the importance of these two pathways, which are crucial for follicular maturation. We believe that a better understanding of the influence that the various ovarian stimulation protocols have on these critical molecular cascades will be invaluable in choosing the best approach for a given patient, thereby avoiding cancelled cycles, reducing frustration and potential treatment-related complications, and increasing the pregnancy rate. Moreover, individualizing the treatment plan will help clinicians to better coordinate assisted reproductive technology (ART) programs, discuss the specific options with the couples undergoing IVF, and alleviate stress, thus making the IVF experience easier.

Background/Aim: Sperm cells are competent to integrate exogenous DNA into their genome. We sought to clarify Human Pappiloma Virus (HPV) internalization in spermatozoa and early preimplantation embryos. Materials and Methods: Sperm was incubated with plasmid vectors containing the complete genome of human HPV 16 and HPV 18 tagged with the green fluorescent protein (GFP) gene, to investigate HPV 16 and HPV 18 integration in mouse spermatozoa. Oocytes were in vitro fertilized with preincubated spermatozoa to investigate HPV 16 and HPV 18 potential transfer to mouse embryos. Results: Spermatozoa were able to internalize constructs of cloned high-risk HPV either as integrated or as episomal DNA. Constructs of cloned HPV can also be transferred to mouse embryos, through in vitro fertilization of the oocytes by mouse spermatozoa. Conclusion: Viral DNA transmission to the early mouse embryo via sperm, highlights the effect of HPV in reproductive cells and preimplantation development.Human Pappiloma Virus (HPV) is a non-enveloped, circular, double stranded DNA virus (1). The viral genome consists of a regulatory non-coding long control region, an early region encoding for E6, E7, E1, E2, E4 and E5 genes and a late region encoding for L1 and L2 genes (2). HPVs are generally classified as low and high risk, according to their potential to cause genital cancer. The different types of papilloma viruses exhibit characteristic tropism and distinct life cycle features (3).HPV 16 and HPV 18, as oncogenic types, are responsible for cervical cancer, the second most common cause of cancer-related death worldwide (4, 5). HPV 16 is considered to be the most frequently identified high-risk HPV genotype, followed by HPV 18. Approximately 70% of cervical cancer cases are linked with these two genotypes (6, 7).Cancer of the uterine cervix is associated with high-risk HPV presence and increased HPV E6/E7 oncogene expression (8-11). Persistent infection with oncogenic HPV genotypes triggers HPV DNA integration into the host genome, eventually leading to chromosomal damage accumulation and genome destabilization in infected cells (12)(13)(14)(15)(16)(17). The exogenous DNA insertion into the oocyte by sperm (18-20), as well as the mechanisms involved (21-28), have been extensively studied. In fact, living spermatozoa of almost all species are able to take up spontaneously exogenous DNA and internalize a part of it into their nucleus (24). The exogenous DNA fragments are localized at the postacrosomal and equatorial regions of the sperm head (22,23) with 15-22% internalized into the sperm nuclei (24). A proportion of the internalized DNA is integrated at specific sites in sperm genome, probably at a nucleosomal subfraction of chromatin, suggesting a common site for exogenous DNA insertion (29,30). Sperm has the capacity to actively take up exogenous DNA derived from HPV. In addition to HPV L1 gene, sperm probably take up DNA from HPV types 16 and 18 (31, 32).Taking into account the capability of sperm cells to integrate exogenous DNA into th...