HPV and Cervical Cancer - Essay Example

HPV and Cervical cancer Affiliation: Introduction There are approximately 40 types of HPV, 30 of which infect the genital tract. There is a strong association between particular oncogenic (high risk) strains of HPV and cervical cancer. Despite the fact that HPV is essential in the transformation of cervical epithelial cells, it is insufficient cofactors and several cofactors and molecular events determine if the cervical cancer will manifest itself. Detecting and treating lesions early can curb cervical cancer from developing in patients with persistent HPV infections. However, cellular abnormalities are often missed resulting in high risk of contracting cervical cancer. This paper seeks to determine the origin and history of HPV, its etiology and pathogenesis, treatments and major symptoms (Bosch & Manos, 2005). The paper will also discuss the demographic attributes of the diseases such as prevalence of certain cultures, gender and age brackets, whether it endemic or epidemic among other issues. Historical Relevance of HPV HPV has been around for more than 100 years. The Scientist tried to establish how the virus evolved to what is known today as HPV. Many years ago, a relative of the virus made dinosaurs sprout warts. When man’s ancestor split from the apes more than 7 million years ago, the virus split with them. The virus then spread and multiplied, evolving to different strains that are present today. Today, the virus which is perhaps the oldest to affect man kind, causes more suffering than it did millions of years ago. The virus still causes warts and cervical cancer, an idea that was suggested more than three decades ago by Harald Zur Hausen, a German scientist. The link between HPV and cervical cancer was documented in the second century by a Greek gynaecology named Soranus of Ephesus. The death rate has since increased because HPV is prevalent in women and they live longer, which gives more time for HPV to advance and form cancerous cells in the cervical region (Bosch & de Sanjosé, 2002). Currently, modern genetics scientists track down the ancient origins of HPV and device means to fight the virus. A Scientist can compare the material in the viruses and draw up a family tree that will help trace the origin and evolution of the virus over time. This way, they will understand the genetics of the virus and determine ways of weakening it or destroying its genetic make-up. Research reveals that there are more than 100 types of HPV, and they all are made up of a scrap of genetic material (DNA), wrapped in a spherical shell of proteins. A keen study of the genetic make-up of the bacteria can reveal more insight on how the virus can be suppressed through altering its DNA (Burd, 2003). Epidemiology The infection is more prevalent in women especially those that start sexual activities at an early age. Research shows that more than 50% of sexually active individuals contact HPV. However, the virus may just stay in the body without causing harm for many years. Only a small percentage of people who contact the virus show symptoms at early stages. The risk for infection and complications is high in women especially those who become sexually active below the age of 25 years. The disease is pandemic and may affect people in all regions and countries as long as they are sexually active. However, the rate of prevalence is high for women who face a high risk of contracting cervical cancer if they persistently contact the virus for a long time (Andrei, Snoeck & Piette, 2008). HPV is not an emerging disease, it has been around for more than a million years, having been transferred to humans when men ancestors split with the apes. The disease was initially transmitted from the dinosaurs, who had a high prevalence for sprouting warts. Over the years, research and scientists notice that some strains of HPV such as HPV 16 have high risk for causing cervical cancer among women. The risk of contracting cancer increased in current times because women’s life span increased, causing the virus to persist in the genital areas, multiply and thereby cause cervical cancer. Although women face risk for cancer, men also contract the virus. However, men are mostly carriers and the virus manifest itself to serious symptoms that endanger health on rare occasions. Etiology of HPV HPV is spread through skin-to-skin sexual contact and is prevalent in all sexually active people, both men and women. The Centre for Disease Control approximates that more than 50% of all sexually active people will contract the virus. Sexual activity is the main mode OF transmission of the HPV. Although condoms may be used to prevent transmission of sexual infections, it doesn’t prevent all HPV infections. A research by the centre for diseases and control revealed that condoms may not protect cervical infection but offer protection against HPV-related infections. HPV is not hereditary and is transmitted through sexual contact (Bonnez & Reichman. 2000). Most people who have the infections become carriers who become the host and transmit it to others through sexual contact. also be spread from the mother to the child during birth, but this is rare. Other modes of transmission include shaking hands with a person infected with warts and sharing contaminated objects. Blood transfusion with infected blood can also cause HPV infection. Surgical procedures on an infected person can lead to its transmission to surgeons and hospital attendants in the operation theatre. There are other factors that increase the infection of HPV. Smoking has been identified as a root cause of HPV infection. Smoking increases the high risk of contracting HPV and the resulting cervical cancer. Women who smoke face a high risk of developing cervical cancer from HPC infection than women who don’t smoke. Having multiple sexual partners is another risky behaviour that increases incidences of cervical cancer. Multiple sexual partners transmit different types of HPV viruses resulting in an increased rate of contacting high-risk types of HPV such as HPV 16 that have high prevalence for causing cervical cancer (Schiffman, Castle & Jeronimo, 2007). Use of contraceptives is also linked to HPV infection. It has not been established exactly how contraceptives increase a person’s susceptibility to HPV infection. However, it is believed that contraceptives increase the frequency of sexual activities, which increases the risk of infection since sexual contact is the primary mode of HPV transmission. Pathology and Pathophysiology HPV infection is restricted to basal cells of the stratified epithelium, which is the only body tissue where they can replicate. The virus doesn’t bind to live tissue but infects the epithelium tissues via micro-abrasions and other epithelial traumas. The infections and micro-abrasions expose sections of the basal membrane, increasing the risk of infection and formation of cancerous cells. The process of infection is normally slow and steady, taking between 12-24 hours for initiation of transcription (Bosch, Manos, Munoz & Sherman, 2005). Scientists believe that antibodies play a critical role in neutralizing the virions while they still reside in the basement membrane and cell surface, which slows the process of infection. The HPV lesions result from the proliferation of infected keratinocytes. The infection often results from exposure of the host’s basal cells to infectious virus. This process occurs through the disturbance of the epithelial barrier that occurs during sexual intercourse or after minor skin abrasions. HPV infections are not cytolytic, rather, release of viral particles leads to degeneration of desquamating cells, that increase risk of infection. The virus a can survive for many months in low temperatures without a host. Therefore, a person with plantar warts can transmit the infection by walking barefoot. HPV is a tiny DNA virus with a genome of 8000 base pairs. Its life cycle follows a differentiation sequence of the host keratinocyte. The cycle involves a series of activities that lead to infection. The process involves the HPV virion affecting the epithelial tissues via micro-abrasions. The virion then associates with putative receptors for example alpha integrins and laminins among others. The association results in the virus entering the basal epithelial cells via clathrin-mediated endocytosis and/or caveolin-mediated endocytosis, depending on HPV type involved. The viral genome is at this point transported to the nucleus, and it replicates itself in the cells (Beaudenon, Kremsdorf & Obalek, 2007). A complex transcriptional cascade occurs as the host keratinocyte starts self-division and become increasingly differentiated in the upper regions of the epithelium. There are two key oncoproteins that are high risks and mainly cause cancer i.e. E6 and E7 proteins that result in high risk of cervical cancer in women. The carriers are asymptomatic and may not show symptoms of infections. Symptoms of HPV A majority of HPV infections do not show any symptoms and hosts are normally asymptomatic. However, persistent infection with specific types of HPV especially types 16 7 18 result in precancerous lesions. These lesions if left untreated may progress to cervical cancer although this progression may take many years. For example, a woman may contract HPV at age 25 but contract cervical cancer at an advanced age of 55 years because it takes time for precancerous lesions to progress to cervical cancer. The major symptoms include the appearance of genital warts that persist for a long periods. The warts may affect all the genital areas, fill with pus and become very painful, rendering the patient immobile (Allen & Kalantari, 2006). The warts may also spread to other areas in advanced stages of infection such as thighs, back and hands, which increases the risk of infecting others. Irregular inter menstrual or abnormal vaginal bleeding after sexual infection may occur in infected women. Patients also experience back, leg and pelvic sharp pain, feel fatigue and loss weight due to loss of appetite. In more severe cases, women may experience vaginal discomfort and odorless discharge that is persistent over time. Swelling of a single leg is also a common symptom for both men and women. Treatment There is no known treatment for the virus itself, but treatment is available for problems caused by HPV. Visible genital warts may remain the same, become numerous or disappear on their own. They can be removed by the patient with proper medication. A care provider such as a gynecologist can also treat the warts. However, mild symptoms of the warts disappear on their own, and medical treatment is unnecessary. Abnormal cervical cells that result from persistent infection with HPVA are identified through a pap test. The cells normally progress to cervical cancer and need to be treated as soon as they are detected. Medicine is administered to suppress their growth and kill them before they develop into full-blown cancer (Adam, 2002). Cervical cancer that results from progression of the precancerous cells is treated by administering cancer medicine to stop growth of cancer cells. Radio therapy and chemotherapy sessions also help to kill cancer cells and treat the disease especially in its advanced stages. Recurrent respiratory papillomatosis is a condition the warts grow in the throat. It is treated through surgery of administering relevant medicine to completely heal the infection. Conclusion HPV is a viral infection that is primarily transmitted through sexual intercourse. Other modes of transmission include shaking hands with a person with open warts, sharing infected objects, prenatal transmission and blood transfusion with an infected person. HPV is an epidemic disease that affects both men and women who are sexually active. Women face higher risks of infection especially initiation of sex at an early age, smoking and use of contraceptives. In advanced stages, HPV causes cervical cancer among women. Major symptoms include genital warts, intermenstrual bleeding, vaginal discomfort, back leg and pelvic pain. There is no known treatment for the virus itself, but treatment is available for problems caused by HPV such as warts, abnormal cervical cells, cervical cancer and recurrent respiratory papillomatosis. References Adam, E., Z. Berkova, Z. Daxnerova, J. Icenogle, W. C. Reeves, and R. H. Kaufman. (2000). Papillomavirus detection: demographic and behavioral characteristics influencing the identification of cervical disease. Am. J. Obstet. Gynecol. 182:257-264 Andrei, G., R. Snoeck, J. Piette, P. Delvenne, and E. DeClercq. (2008) Antiproliferative effects of acyclic nucleoside phosphonates on human papillomavirus (HPV)-harboring cell lines compared with HPV-negative cell lines. Oncol. Res. 10:523-531. 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