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Oncogenic Viruses

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Oncogenic Viruses
Human oncogenic viruses are viruses that can cause cancer. Today, a substantial amount
of cancer cases worldwide, about 12% of all cancer cases, has viral infections as an underlying
cause. According to medical experts, the human oncogenic viruses are the following: “human
papillomaviruses (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), EpsteinBarr virus
(EBV), Kaposi’s sarcoma-associated herpesvirus (KSHV) (also called human herpesvirus 8),
human T-cell lymphotropic virus (HTLV-1), and Merkel cell polyomavirus (MCPyV)” (Schiller
& Lowy, 2020). As for this data, it is worth mentioning that such conclusions required a significant
amount of clinical research and trials over the past fifty years. However, contracting a viral
infection with one of the previously mentioned infectious agents does guarantee cancer. For
instance, a specific microenvironment is required for oncogenesis to take place. Consequently, an
interplay between the immune system of the host and the molecular mechanism of the virus is
needed (Mui, Haley, & Tyring, 2017). This paper will mainly focus on the human papillomavirus
(HPV) and the hepatitis B virus (HBV).
To begin with, HPV exhibits manipulation of usually occurring signaling pathways. The
PI3K-AKT-mTOR pathway is a prime example of a mechanism hijacked by an oncovirus. In a
normal case scenario, this signaling pathway is important for normal cell growth, survival, and
proliferation. Hence, the dysregulation of the PI3K axis will disturb physiological maturation and
promote tumor cell growth instead. In the absence of the necessary growth factors for this tract,
HPV evolved molecular mechanisms that can engage this pathway regardless. HPV possesses what
is known as an oncoprotein. Those proteins are E5, E6, and E7, which predispose infected cells to
tumorigenesis. Another signaling pathway HPV can hijack is the MAPK signaling pathway.
Disrupting MAPK signaling will benefit the infected cells with invasive properties thus, enhancing
the metastatic capabilities of the oncogenic cell (Krump & You, 2018). Unfortunately, signaling
pathways are not the only mechanism disrupted by HPV; the latter can also exploit the host’s DNA
damage repair mechanisms. Under normal physiological conditions, DDRs have two main
signaling networks: ATM (ataxia telangiectasia mutated) and ATR (ataxia telangiectasia and
Rad3-related protein). Those signaling networks regulate the activity of p53, which is one of the
most vital tumor-suppressor proteins. HPV, a DNA virus, will activate ATM and ATR-related
DDR factors and recruit them, thus, boosting viral DNA replication (Krump & You, 2018). The

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primary purpose behind this molecular mechanism is for the virus to enhance the chances of adding
more carcinogenesis-associated mutations to their genome. Finally, HPV can manipulate the
immune response of its host. This tactic will allow the virus to evade the defense mechanisms of
the host. Thus, the oncogenic virus will survive longer and cause more harm in the infected cells
(Krump & You, 2018).
The hepatitis B virus or HBV exhibits similar molecular mechanisms as HPV. However,
the former will employ different oncoproteins and different virulence factors. For instance, HBV
also can target host signaling pathways, exploit the DNA damage response of the host, and
manipulate immune responses. To begin with, HBV targets host signaling mechanisms by
activating the Notch-signaling pathway. The oncogenic virus will make use of the HBx protein to
induce the expression of NOTCH1. The latter will enhance the proliferation of hepatocellular
carcinoma and increase the predisposition to HBV-associated hepatocellular carcinoma (HCC).
Then, HBV exploits host DNA damage response by degrading the structural maintenance of
chromosomes complex five and six. Under normal physiological conditions, SMC5/6 would
repress HBV viral transcription. However, with the help of its viral protein HBx, HBV will degrade
this complex. Thus, HBV increases its viral gene expressivity and replication. Finally, the hepatitis
B virus manipulates the host immune responses via its HBV polymerase. The latter interacts with
the stimulator of interferon genes (STING) to stop the transcription of the interferon regulatory
factor (IRF3) which, drives immune response against oncogenic DNA viruses. Another way HBV
can stop IRF3 transcription is via the combined effect of HBx and HBV polymerase on the host
cell’s Toll-like three receptors (TLR3). Thus, by inhibiting interferons, the virus increases its
chances of evading immune response and survival (Krump & You, 2018).
To wrap it all up, the discovery of oncogenic viruses had a massive impact on medicine as
we know it today. Because understanding the molecular basis behind the pathogenesis of those
oncogenic viruses is essential to diagnose and treat viral cancers. In the past, physicians could not
determine the etiology of the diseases caused by those viruses. However, with all the recent
advancements in clinical research, diagnosis and treatment are much more feasible. But treatment
is not always possible since oncogenic viruses keep evolving and developing new strategies.
However, with the fast-developing technologies, research on host-virus interaction is much easier.
Yet, one may still ask, will we ever be able to outpace tumorigenesis and put an end to this disease?

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Oncogenic Viruses Human oncogenic viruses are viruses that can cause cancer. Today, a substantial amount of cancer cases worldwide, about 12% of all cancer cases, has viral infections as an underlying cause. According to medical experts, the human oncogenic viruses are the following: “human papillomaviruses (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein–Barr virus (EBV), Kaposi’s sarcoma-associated herpesvirus (KSHV) (also called human herpesvirus 8), human T-cell lymphotropic virus (HTLV-1), and Merkel cell polyomavirus (MCPyV)” (Schiller & Lowy, 2020). As for this data, it is worth mentioning that such conclusions required a significant amount of clinical research and trials over the past fifty years. However, contracting a viral infection with one of the previously mentioned infectious agents does guarantee cancer. For instance, a specific microenvironment is ...
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