The Early Viral Genes ( E6 And E7 )

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The early viral genes E6 and E7 can influence both replication and transcription of the virus, and also interacts with host regulatory proteins [2]. Upon infection of the host, the viral genome ring is disrupted leading to its ability to incorporate its genome into that of the host's [2]. Once the viral early proteins interact with the host’s regulatory proteins, the host cells will lose function of regulating tumor suppression, ultimately stimulating the proliferation of the HPV infected cells [2][7]. Papillomaviruses tend to replicate within cells through the lysogenic pathway, and incorporate its viral genome into the host’s genome [7]. Stated earlier, early detection of this particular virus is challenging because the
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These early genes, can exhibit their functions alone, but their functions are stronger and more efficient when they are in combination with each other [4].
Early Genes E6 and E7 Both early genes E6 and E7 are responsible for the progression of cervical cancer oncogenesis [2][4]. These two genes have many different actions but discovered first was the interaction that E6 had with p53 and how E7 interacts with RB, both genes will initially alter host metabolism to favor abnormal cell development [4][7]. By degrading host p53, the host cell can no longer initiate apoptosis upon infection [7]. P53 and RB have crucial roles in the cell maintainence of the cell cycle specifically at the (G1/S-phase checkpoint) [7]. Explain their role and importance in cell processes.
Following its initial interaction with p53, E6 also interacts with another pro-apoptotic protein, BAK [4]. E6 with its known interactions with p53 and BAK proteins, will ultimately affect the process of apoptosis of abnormal or damaged cells leading to an increase in chromosomal damage and proliferation of the damaged oncogenic tissue cells [4]. The proliferation of this tissue is also enhanced when E6 oncoprotein activates telomerase and SRC kinases that stimulate cell growth [4][7]. The protooncogene SRC kinases have been speculated to contribute to the transformation of the HPV phenotype on epithelial and mucosal

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