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Human papillomaviruses are considered to be Group I viruses according to the Baltimore classification sytem. This is determined by looking at the genome type of the virus. When virus particles were isolated from humans, scientists were able to see that the viral genome had a double stranded circular DNA molecule (Arrand 28). The protein capsid of the virus has an icosahedral shape (T=7) that measures approximately 55nm in diameter (Syrjanen 2). The human papillomavirus contains several different important proteins. These proteins can be divided into two groups: early and late. The early proteins consist of E1, E2, E4, E5, E6, and E7, while the late proteins consist of L1 and L2 (McCance 33). Each protein is important because they all play an important role in gene expression and replication.
To even become infected with human papillomavirus, the virus must make its way into your body and to your cells. The first step is attachment, in which the virus can only attach to non-differentiated basal cells of stratified squamous epithelial or mucosal tissue, usually in a microwound. At least 30 different types of HPV is associated with infecting the genital tract. Certain HPV types such as HPV 16, which is one of the leading causes of genital cancer, require Î±-6 integrin as the main receptor in order to attach. Once attached, the virus can enter the cell via endocytosis. The virus then uncoats as the circular genome enters the cytoplasm as an episome. An episome can freely replicate independently or become part of the cell's chromosome. The DNA then moves into the nucleus where it can express genes and replicate. The first genes to be expressed are the early genes, E1 and E2. For example, the E1 protein is required in order for viral DNA to replicate. E2 is also required for replication, thus working together with E1. It is also involved in transcriptional regulation. E4 proteins are still somewhat a mystery in regards of its primary function. However, studies have suggested that it may play a role in a collapse within the cell, resulting in the virus being able to be released from an infected cell. E5 is very significant, because it has been discovered that it is somehow responsible for transforming cells in culture. Two important early genes, E6 and E7, are the proteins that have been linked to causing cancer. E6 has been linked to inactiving p53, which is an anti-oncogene. E7 also reacts with another anti-oncogene called Rb. These interactions cause interference with the anti-oncogenes, which lead to forcing the cells to replicate and divide rapidly. Differential, rapid cell division can have cancerous effects because of the likelihood of something going wrong with each division that occurs. The interaction between E7 and Rb is significant, because it results in accumulation of cell damage. During replication, the virus uses the cell host's resources such as enzymes in order to replicate. The first step involves the virus infecting the basal epidermal layer. The virus replicates until there is around 50-100 genome copies inside each host cell. In the second step, the virus then only replicates according to the host cell cycle. The final stage involves a large increase in copies of viral genomes along with the late genes being expressed, which is involved with forming the capsid for the genomes. The L1 protein is responsible for encoding the icosahedral capsid that can be found around the genome. Lastly, the L2 protein also plays a role in forming the capsid, but not as significant as L1. L2 is more complementary in which it stabilizes the capsid (Arrand 36). The virus is then assembled inside the nucleus and then leaves the cell via cell lysis. During cell lysis, the host cell is burst open and all the viruses leave to go infect other cells.
Human papillomavirus infection occurs when the virus enters the body through a cut or lesion on the surface of the skin. HPV can affect both males and females. Transmission of HPV can happen with any skin contact, especially in the genital areas with someone who has the virus. However, intercourse might not always necessary. There are over one hundreds types of human papillomavirus that can cause infections to human. Of these hundreds there are more than forty types that can cause genital warts. Some HPV types also cause the common warts on the hands, feet (plantar), and other lesion in the mouth and upper respiratory system. The signs and symptoms that do appear may vary according to the type of HPV infections. Many people infected with HPV might not even realize that they have it because the virus often has no signs or symptoms. Therefore, someone who gets the virus might pass it to his or her partner without knowing it. In most cases, the body natural defense system will fight off the virus and the virus will clear on its own. However, in the case when the body defense mechanism cannot fight off the virus, HPV can then cause visible changes in the form of warts. Although most infections or the common warts cause no symptoms, the persistent of genital wart infection can cause cervical cancer in women. Warts usually appear weeks or months after the person accoutering with the virus. Warts have many morphology it can be raised, flat, or even cauliflower shape. In case of cancer, it often takes years to develop.
Moreover, human papillomavirus have been further classified as either "low risk" or "high risk" based on the pre-neoplastic character of the clinical lesions with which they are associated. Low-risk HPVs such as HPV-6 and HPV-11 are generally associated with venereal warts or genital warts, which only rarely progress to malignancy. The high-risk HPVs include HPV-16 and HPV-18 that are potentially precancerous.
More than a century ago sexual activity was already considered as an important risk factor for the development of cancer of the uterine cervix or cervical cancer, the second leading cause of deaths of cancer among women worldwide. Epidemiologic studies have implicated a sexually transmitted agent as a case of cervical cancer, and molecular virology studies over the past ten years have established a strong association between specific human papillomavirus types and certain anogenital carcinomas, including cervical cancer and other cancer of the vulva, anus, or penis. Candidate microorganisms that have been critically studied include bacteria (Treponema pallidum, Neisseria gonorrhoe, Chlamydia trachomatis), protozoa (Trichomonas vaginalis), and viruses (herpes simplex and cytomegalo virus), but these appear to be of minor importance. Since 1970, the possible involvement of human papillomavirus infections in the etiology of human genital cancer has been under investigation. Originally, a single human papillomavirus was believed only to cause benign skin warts, papillomas, and warts on the genitals (condylomas). However, in 1976 Zur Hausen pointed out that genital warts show an identical epidemiological pattern as cervical cancer and postulated that a papillomavirus could be involved in the development of cervical cancer.
The transmission of human papillomavirus can vary between different people. In cases where sexual activity is involved, HPV can be transmitted through both anal and vaginal intercourse. They can also be transmitted by skin to skin contact and also through oral sex. In non-sexual situations, HPV transmission can occur through the mother passing it on to a child during birth, which is rare, and also by regular skin to skin contact. However, transmission of HPV can be reduced and even prevented if the right precautions are taken. Vaccines are used to prevent becoming infected with certain types of human papillomavirus. The two most popular vaccines, Gardasil and Cervarix, are widely used to prevent HPV type 6, 11, 16, and 18. These 4 types of HPV account for 90% of cervical cancer (Frey 2010). The vaccines are effective for both males and females between the ages of 9 and 26. To prevent, transmission via sexual contact, wearing a condom can be effective in reducing skin to skin contact. Warts that have developed as a result of HPV normally go away on their own. However, they can be removed either physically or by freezing them. Abnormal cells can be detected by going to a doctor and performing a PAP smear. Along with using this Pap smear method, smoking should also be avoided to decrease the likelihood of developing cervical cancer.
In the United States, human papillomavirus is considered to be one of those most acquired infections via sexual contact. Therefore, it is not surprising that the virus is widespread and affects many different groups of people. After all, there are many different strains of HPV that could potentially infect an individual. However, in some certain demographics, infection caused by the virus is more prevalent than others. The most significant factor with regards to HPV infection is the sexual behavior of an individual. For example, a study shows that HPV infection among males who do not engage in sexual were almost non-existent. On the other hand, HPV detection shot up to 43% in males who did engage in sexual activity (McCance 8). Studies have also shown that young sexually active women to be most likely to experience HPV infection. A common trend observed with infection rate is that the increase of STD cases was proportional to the increasing number of young and sexually active people. Most studies show that the prevalence of HPV hits its peak in age groups of 16 to 25. The prevalence of HPV among people gradually decrease with increased age, which is most likely be attributed to a healthy immune system working against and clearing out HPV infection (Mayo Clinic).
Human papillomavirus which can lead to cervical cancer accounts for over 400,000 cases per year worldwide with an estimated of at least 200,000 deaths. Another factor, which can lead to increased number of HPV cases is smoking. A person that smokes are also more likely to develop cervical cancer because smoking down regulates the immune system, which increases a person's likelihood of developing HPV infection. Despite HPV infection being common, the availability of pap smear screening has helped with testing and detection of abnormal cells to help prevent cervical cancer, thus lowering the mortality rate caused cervical cancer. This test might not be available in developing countries without adequate resources, therefore it is apparent that most mortalities from cervical cancer caused by HPV infection are outside of the United States (Hausen).