Write a paper on the role of infectious agents in oncogenesis. Use the below as your guideline.
- Introduction and history of infectious agents and oncogenesis-
- Identify at least five (5) infectious agents that play a role in oncogenesis-
- For each infectious agent, discuss the following;
- What cancer (s) is it associated with its development?
- What is(are) the oncogenic factor(s) in the infectious agent?
- What is(are) the mechanism(s) of oncogenesis-
- What are your suggestions for prevention, control and or treatment of any of these cancers?
Role of Infectious Agents in Oncogenesis – Sample Paper
The initial idea that viruses contain a role in malignancy etiology was first introduced in 1911 by Peyton Rous publication, who claimed that a cell extracted from a chicken tumor contain filterable agent which could spread the tumor to healthy chicken (White 464). Since then, there has been extensive growth and advancement in epidemiology and biology fields such that, researchers have in the 20th century clarified casual relations between malignancies and specific infections agents. Accumulating evidence from the beginning of 20th century demonstrates that some infections might be directly connected to incidences of cancer. Infections are currently associated to around 15 to 20% of cancer cases in the world. This value is considerably higher in developing countries where cases of infections are very high. Infectious agents are said to increase cancer risk through different mechanism which include destroying the DNA of the host cell directly by stimulating processes of mitosis or by introduction of active oncogenes, inducing immunosuppression, and chronic infection (Jacqueline 1).
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researchers have today identified various infectious agents that play a role in
oncogenesis. Some of these infectious agents include H. Pylori, Human
papillomaviruses (HPV), Epstein-Barr virus (EBV), hepatitis B virus, and human
T-cell leukemia virus type I (HTLV-1).
Pylori (H. Pylorin)
is a bacterium which gets through human body through oral-fecal route, via
contaminated water and food. H. pylori are responsible for gastric cancer,
peptic ulcers, and chronic gastritis. The research has clarified significant
host factors and bacterial which are responsible for gastric malignancy and
gastric inflammation induced by h. Pylori. The cytotoxin-related H. pylori
antigen A is the main oncogenic element injected into the cells host from
bacteria and it disrupts functions of epithelial cells. H. pylori initiate
epigenetic alterations including DNA histone and methylation modification (Ding
et al 5). The best way to prevent h. pylori is by ensuring personal hygiene
which includes cleaning hands with soap after visiting the toilet, ensuring the
food is cooked well and ate when hot and ensuring drinking water is free from
leukemia virus type I (HTLV-1).
Human T-cell leukemia virus type I (HTLV-1) refers to a retrovirus which induces CD4+ T cells, ATL malignant disease. This virus is highly responsible for blood cancer commonly regarded as Lukemia which involves attack on white blood cells. HTLV-1 is spread through sharing needles, sexual contact, and blood transfusions. After transmission, proviral DNA is generated by reverse transcriptase from genomic viral RNA. Provirus is then integrated by viral host genome. After this HTLV-1 infection is said to spread via cells division, with least production of particles. The best way to prevent this HTLV-1 should be through proper screening to avoid transfusion related form of transmission. Prenatal screening should also be done to prevent transmission of the virus to the child from the mother (Goncalves et al. 585).
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HPV is a
virus which is the main cause of cervical cancer. One possible mechanism of
this interaction might depend on products of C. trachomatis which might
influence immunity permitting the persistence of oncogenic. Other risk factors
include multiple sexual partners, early age sexual intercourse, poor immune
system and smoking. One of the main HPV-induced carcinogenesis events is the
HPV genome integration into the chromosome of the host. Integration of HPV genome frequently occurs
close to common fragile human genome sites. Integration normally follows an
extra specific pattern with regard to the HPV genome. In this particular case,
the viral E7 and E6 genes expressions are maintained consistently while other
viral DNA portions expression is disturbed or the entire DNA deleted (Munger et
al. 11453). HPV can be prevented by use of condom, and sticking to one sexual
EBV is a virus that is transmitted through shared utensils, sneezing, coughing, and kissing. The virus is highly associated with nasopharynx and lymphoid cancers. The EBV virus is introduced in the B cell lines. The EBV changes B cells into immortalized cell lines. The viral DNA in latent infection is stably upheld as extrachromosomal episome using a unique plasmid DNA origin replication which is activated by binding EBV nuclear antigens (Raab-Traub 3). The best way to prevent the EBV infection is by keeping off infected people and ensures that one does not share their personal items including glasses and silverware with them.
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B virus (HBV)
HBV refers to a
minute enveloped DNA virus which is responsible of chronic and acute hepatitis.
The virus is transmitted through needle sharing, transfusion, prenatal
transmission, unprotect sexual contact, and breastfeeding. HBV is highly
responsible of liver cancer. In the chronic hepatitis B progression from the
state of asymptomatic carrier to HCC, accumulation of mutations happen at the
viral genome in the region of preS. Thus HBV is normally involved in the
alteration of the liver cell in chronic hepatitis resulting to genetic alterations
mutations (Neuveut et al. 597). The HBV
preventive measures should thus include effective blood screening before
transfusion, using condom during sexual intercourse, and maintaining one sexual
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