The Cell Via Clathrin Mediated Endocytosis

HeLa cells have had a positive influence on medicine in many ways including with giving us knowledge about the human papillomavirus (HPV) DNA and HPV18-positive. HeLa cells have been linked to changes in microRNA expression. Since HPV18 has been associated with very aggressive adenocarcinomas, this finding may explain why Dr. Gey was surprised by the prolific growth of HeLa cells in culture. Routine Papanicolaou smear screening may not detect rapidly progressive cervical carcinomas; the new HPV vaccine holds the promise of preventing these tumors. (Hutchins).

Cervical cancer is the leading cause of cancerous death, in women, since 1950. Approximately 200,000 cervical cancer patients die each year in developing countries. Strains like HPV 16 and 18 cause about 70% of cervical cancer in women– one of the top causes of death in the world (WebMD, 2010, p.1). In the Unites States, about 10,000 women acquire the disease and 3,700 die annually Human Papilloma Virus (HPV) is directly associated as a cause of cervical cancer. This virus affects the skin and genital area and, in some cases, it can also infect the throat and mouth. Since the HPV is passed from one person to another through skin-to-skin or sexual contact, sexually active people are more prone to this virus. Merck

Human Papillomavirus (HPV) is a double -stranded deoxyribonucleic acid (DNA) virus that only infects humans with an attraction to both cutaneous and mucosal surfaces such as the cervix, anus, tonsil, and oropharynx (Clark, 2013). HPV is a type of oncogenic virus that goes into the cells and can cause several diseases. Over the years, research has surfaced connecting genital HPV to several types of cancer. There are over a hundred strains of HPV but the most high risk strains, 16 and 18, have been shown to cause vulvar, vaginal, anal, and the most concerning, cervical cancer (Chan, Ng, & Wong, 2012). Genital HPV

Human papillomavirus (HPV) is made up of double stranded DNA with a capsid. Their viral genome is consisting of such as early (E) gene like E6 and E7encodes for oncoproteins and late (L) gene such as L1 and L2 encodes for structural proteins like capids. There are more than 100 different types of HPV identified and they generally infect around cutaneous or mucosal areas. HPV viral genome can be categorized into low risk (LR) and high risk (HR). High risk types such as HPV-16 and -18 are ones that can develop into cancer and other tumors mostly in genital area or a head and neck squamous cell. Low risk types such as HPV-6 and -11 are more frequently found I larynx or genital area (Klozar et al., 2010). Therefore, careful evaluation such as risk factors, or possibly a new vaccination to prevent against HPV related to oropharyngeal SCC should be questioned in public health

Human Papilloma Virus (HPV) accounts for the third most prevalent cancer in females worldwide,15 as it is the most common sexually transmitted infection (STI).2 There are more than 100 subtypes of HPV; 16 of those subtypes are known to be high-risk.15 HPV is a crucial precursor to cervical cancer in 99.8% of those affected,2 with subtypes 16 and 18 being the most common types.15

Human Papilloma Virus (HPV) is a double stranded DNA virus. There are many genotypes HPV and some of them are oncogenic. They have envelope proteins E6 and E7 on their cell wall which are associated to initiate cancer. Anogenital lesions associated to HPV are divided into ‘low-risk’ types (6, 11, 34, 40, 42, and 43) and ‘high risk’ types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 69, 73, and 82). Most of the low risk HPV infections are asymptomatic and are not fatal, however infection to high risk HPV such as type 16 and 18 may cause cervical, anal, vaginal, vulvar and penile cancer (Centre of Disease Control, 2012). Low risk HPV generally cause warts on the skin surface which rarely develop into malignancy. Type 16 and 18 both were originally isolated from cervical carcinomas of human body. More than 70% of human cervical is due to the infection of either HPV 16 or 18. According to CDC, in 2008 it was estimated 11,070 cases of cervical cancer in United States and about 3,870 deaths due to cervical cancer. Higher percentage of HPV persistent infection occurs by HPV-16 and the risk of getting cervical cancer due the progression of disease is higher for HPV 16 and 18 and 45 (Tino F. Schwarz, 2008).

HPV works like all other viruses, the virus inserts its DNA into the cell and the cell begins to produce the protein that the virus encodes. HPV attacks epithelial cells, epithelial cells are what make up the outside layer of skin on the body, including the cervix. In types 16 and 18 the creation of HPV proteins interferes with the cell’s ability to prevent excessive growth. The cell grows uncontrollably and does not die. This excessive growth is manifested as a precancerous

HPV, an abbreviation for human papilloma virus, is the most common sexually transmitted infection. According to the CDC, about 14 million people in US gets infected with HPV annually (“Human Papillomavirus” CDC). HPV is so common that it infects at least 75% of all people who are sexually active once during their lifetime (“Human Papillomavirus” Canadian Cancer Society). The infection with HPV usually occurs soon after the onset of sexual activity. This paper will cover what HPV is, its effects on the body and prevention.

Papillomaviruses are exceptionally predominant in the set of all animals, however every infection has its own particular assault arrangement. Human papillomaviruses can cause an assortment of therapeutic conditions. HPVs are non-concealed DNA infections that contaminate cells of the skin and mucous layers. A great many people who contract human papillomavirus disease have no side effects, and they rapidly clear the infection from their bodies. In any case, in other individuals certain sorts of generally safe HPVs cause genital warts. Other HPV sorts are the primary driver of cervical malignancy, and are related with butt-centric, penile, mouth, and throat growths. These are alluded to as

Human Papillomavirus (HPV) is a DNA virus that infects the keratinocytes of human skin and mucous membrane. It is the most common sexually transmitted infection in the world. An estimate of 79 million people in the United States are currently infected with HPV(1). With over 100 types of the virus, at least 40 types can infect the genitalia, mouth and throat. Particularly, HPV-16 and HPV-18 cause approximately 70% of cervical cancers. Transmission occurs through sexual intercourse, but can also occur through non-penetrative sexual activities.

In this method, the binding of the virion to host receptors triggers Clathrin-mediated endoycytosis.The virion attachment to the host receptor causes the binding of an adaptor protein to the receptorcytoplasmic tail. Adaptor proteins bind to clathrin, and the local concentration of adaptor proteins onthe inside face of the plasma membrane allows clathrin to multimerize to form Clathrin-Coated Pit(CCP). GTPase dynamin pinch off the CCP from the host membrane thereby releasing the Clathrin-Coated Vesicle (CCV). Auxilin and hsc70 release the clathrin basket. The vesicle then delivers itsviral content to early endosomes. Endosomal carrier vesicles transport contents of early endosometo late endosome that is near to nucleus. Then, late endosome fuses with lysosome.decrease in pHis due to vATPase ,which is used to pump out protons into vesicle.

The human papillomavirus (HPV) is one of the human viruses that people might not be aware that they have. HPV can be present within someone’s body but there may be no visual signs or symptoms. The reason why there may be no signs and symptoms is because the immune system can diminish HPV on its own since it can automatically sense it and clear it out of the body, this happens about 90% of the time. Vast majority of the people having human papillomavirus will be cleared out within two years and have no future problems. The Oral Cancer Foundation states that HPV might be present in human body for many years before it is detected or converted to something worst such as cancer (N. Sathish, 2014). However, there are cases when the HPV will stay

Rationale: During viral infection, most viral pattern recognition receptors (PRRs) stimulate the expression of type I interferons (IFNs), which are the most potent known antiviral factors and are capable of limiting the replication and spread of most viruses (71-73). Type I IFN not only plays an essential role in defense against papillomavirus infection at any stage of the virus life cycle, it also regulates multiple aspects of innate and adaptive immunity (74, 75). Papillomaviruses evade immune surveillance by downregulating the expression of IFNs in host cells (61-63). For example, HPV16 E6 and E7 proteins are found to downregulate the expression

Human papillomavirus (HPV) is a small, uncoated deoxyribonucleic acid (DNA) virus that is responsible for infecting the skin or mucous membranes. It is circular in shape and has a double-stranded viral genome which is approximately 8 kb long. This genome encodes for early proteins which are six in total and is responsible for viral replication and 2 late proteins, L1 L2 and which are viral structure proteins. These type of viruses are encapsulated in a 72-degree capsid of icosahedral protein. HPV is a group of more than 200 viruses linked to the skin and moist membranes lining of the body like the cervix, the anus, the mouth and the throat.

HPVs are divided into two different categories low-risk and high-risk depending how they behave overtime. ‘High-risk’ mucosal HPVs are the causative agents of cervical cancers, with HPV16 and HPV18 being the most common oncogenic types associated with 50% and 20% of the carcinomas respectively (Bosch et al., 1995). There are two viral protein that causes the degradation of the tumor suppressor genes; E6 and E7. These two protein work together to cause the tumor by destroying the host machinery. E6 oncoprotein has the capacity to block apoptosis, changes the function of several proteins and thereby modifying the signals of the cells. One of the major function of the E6 protein is to target the p53 (a tumor suppressor protein), it inactivates and recruit the E3 ubiquitin ligase E6AP (Huibregtse et al., 1991; Scheffner et al., 1993) by binding to a conserved