Viral Dna, Viral, And Oral, Vaginal And Anal

In today’s society individuals can be affected by a number of different viruses and infections. A virus is defined as “various numbers of submicroscopic parasites that can infect any animal, plant, or bacteria and often lead to very serious or even deadly diseases”. One of the most widespread viruses alive today is the Human Papillomavirus commonly known as HPV. HPV can be spread during any kind of sexual encounter even without penetration; it is most frequently spread by skin-to-skin contact during sexual activity with the penis, scrotum, vagina, vulva, or anus of the infected individual. There are more than a 100 different types of HPV viruses, which can be considered

Human papillomaviruses (HPV) are a group of more than 40 types of viruses that infect the genital areas, throats (recurrent respiratory papillomatosis), and mouths of males and females and is the number one most common sexually transmitted disease (Center for Disease Control and Prevention [CDC], 2009). It is spread by genital contact. It is most easily spread by vaginal and anal sex, but also through oral sex and even just genital-to-genital (skin-to-skin). In 90% of people that contract HPV, their own immune system

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

Our laboratory has developed the mucosal MmuPV1 infection mouse model recently and noninvasive methods to track the infection from oral and anogenital canals longitudinally [14]. Our long term goal is to use this model to explore many unanswered questions regarding viral-host interaction during papillomavirus infection. Innate immunity, a critical part of host defense system, is not only the first line of defense against pathogens, but is also critical for stimulating adaptive immune responses in viral infection [15-22]. Other host defense factors including interferons, Toll-like receptors, cytokines and defensins all play an important role in papillomavirus persistence and progression [23-31]. However, some findings in human studies are inconsistent

HPV lives in the body’s flat and thin cells on the skin’s surface called epithelial cells (“Information About the Human Papillomavirus”). There are more than 200 related viruses

The male sexual is the vector of the HPV infection. Personal interviews were conducted and demographics showed smoking, genital hygiene, circumcision use, and history of STDS. HIV was not tested. The HPV was detected by swabbing the external genital area with cotton swabs, one over the sulcus coronaries of the penis, and the other over the shaft of the penis, the scrotum, and the perianal region. The swabs were immediately placed in the same plastic tube containing 3 ml phosphate buffered saline and 0.005% thiomersal and kept 4 degrees Celsius until mailed for analysis. Next, after centrifugation for 10 minutes at 2755 g, the pellet was resuspended in 100

Human papilloma virus (HPV) is a virus that can cause both cervical cancer and/or genital warts. In most cases of HPV there are no symptoms and individuals are unaware that they have the virus (Centers for Disease Control and Prevention [CDC], n.d.). It can be spread through vaginal, anal and oral intercourse and is the most common STI (CDC, n.d.). In 2006 a vaccine was approved to protect against the types of HPV associated with the majority of cervical cancer and genital warts (Gardasil, 2014). I have found through my clinical experience that many parents are unsure if their child should receive the HPV vaccination. There are many factors including baseline knowledge, safety, effectiveness, cost, values/beliefs

Viral DNA was monitored by collecting lavage or swab samples periodically. Active infection was detected at all the mucosal sites: the penis (P), the anus (A) and the oral cavity (O) at week seven post infection (Fig. 2). The infection persisted in all the sites in these animals.

As mentioned earlier, HPV is a non-enveloped, icosahedral capsid, double-stranded circular DNA virus (Morshed, 2014). Infection of HPV occurs in the cervix, glans of the penis, penile shaft, scrotom and anal verge by interactions with putative “host cell surface receptors such as heparin sulfate proteoglycans and alpha-6 integrins” Schafer, 2015; Letian, 2010). Most studies suggest that HPV16 enters the cell via clathrin-mediated endocytosis (Day, 2003, Bousarghin, 2003, Smith, 2007, Hindmarsh, 2007), however, notably, a few contradictory studies suggest that HPV16 is clathrin and caveolaen independent (Spoden, 2008). Once the virus has entered the cell, it then un-coats and delivers its genome (8 genes) to the host cell nucleus to be expressed. These eight genes are named for when they are expressed during the virus’s occupation of its host: early (E) and late (L). The proteins E1, E2, E4 and E5 play an important role in genome replication (Beutner, 1997; Gnanamony, 2007) while E6 and E7 are oncogenes and are capable of causing cancerous growth of host cell (Gnanamony, 2007; Sikorski, 1998). E6 is thought to complex with p53 which is a cellular tumor repressor (Werness, 1990); when E6 complexes with P53, it is thought to promote the degradation of p53 via the ubiquitin pathway (Schffner et al., 1990). This degradation of p53 contributes to the oncogenic potential of high-risk HPVs (Stewart, 2005, Thomas, 1999). Crook showed that E6 can bind with p53

Human Papillomavirus (HPV) is a sexually transmitted infection with fourteen million new cases per year (Valentino & Poronsky, 2016). These astronomical numbers make HPV “the most prevalent sexually transmitted infection in the United States” (Valentino & Poronsky, 2016). HPV infections have been associated with causing multiple cancers. In 2006, the first vaccine against HPV emerged, Gardisil. In 2009 a second vaccine was approved by the FDA, Cervavix (Valentino & Poronsky, 2016). Despite the development of the HPV vaccine, compliance remains low at an uptake rate of only 37.2% in adolescent females (Cassidy & Schlenk, 2012) and 10-12% in adolescent males (Thomas & Snell, 2013). Lack of education, specifically to adolescents and their caregivers, is in large part a direct contributing factor to decreased compliance.

HPV is the most common sexually transmitted infection (STI) among men and women that may infect the mouth, throat, genitalia and anus resulting to genital warts formation or cancer. (Center

These IFNs induce an antiviral state in both the infected and neighboring cells, and prevent the spread of viral infections (41, 79). With a deficiency in type I or II signaling, host immune cells such as NK cells and neutrophils might not be able to function appropriately and therefore the host might be more susceptible to viral infection. However, Ifnk-/- and ifn-αβR- mice might be resistant to the MmuPV1 infection like NOD/SCID mice at cutaneous sites because of redundancy in these mice. Although it may seem disappointing but this finding will be worthy of additional investigation. Alternatively, we can test other mice deficient for critical IFN components such as MAVS, IRF-3, or IRF-7 that have shown increased morbidity and/or mortality to other viral infections (80). Other antiviral factors of innate immunity including human α- and β-defensins have been reported in HPV-associated anogenital warts (31, 32, 81, 82). We have detected downregulation of β-defensins 4 and 6 in MmuPV1-infected tissues by RNAseq (Table 1). We can explore whether these antiviral factors play a role in MmuPV1 infection. These additional studies will help to sort out the key players in papillomavirus

Understanding of the HPV lifecycle is mainly derived from research on HPV 16. However, with slight modifications, life cycle model of HPV 16 can be applied to other HPV types as well.17 Skin to skin contact is the primary route of transmission, and sexual behavior greatly influences the incidence and prevalence of HPV infections.18 Virus finds its way to basal epithelial cell via micro-abrasions and micro-traumas on the skin. It is not fully understood how the virus binds with the surface of basal cells. However, L1 and L2 capsid proteins, alpha-6 integrin cellular receptors, and heparan sulfate proteoglycans/heparin sulfate may play a role in the process of binding.19 The virus enters basal epithelial cells through endocytosis, and the capsid is disassembled by the cellular endosome/lysosome. The L2 viral protein transfers the viral genome to nuclei of keratinocytes,20 and with the help of early viral proteins (E1 and E2), the virus maintains its episomal form and replicates in synchrony with the host DNA.17 As the infected host cells differentiate, late viral promoters are activated which facilitate viral packaging and release.17,20 Usually the expression of L1 and L2 viral proteins takes place in the granular layer the viral assembly in the cornified layer of the skin.7,20 Viruses are

The human body is made up of many different organs and systems. Each body is different in shape and size. Some bodies function as they should and there are others that are abnormal. The human body has many systems that have specific functions and uses. Some systems that make up the body function on a daily basis include; digestive system, immune system, muscular, and skeletal system. Viruses and diseases affect the body by breaking it down and causing dysfunction. Diseases if not caught early can lead to death or permanent damage in the body. What are diseases and how do they affect the human body? In this paper HIV will be discussed as well as how many are affected in America. Explanations on how the body systems are affected by HIV and the medications and treatments for HIV will be discussed.

There are 4 stages from the initial HPV infection through the development of cervical carcinoma; HPV infection with high risk HPV ,viral persistence infection more than 10 years, progression of a clone of persistently infected cells towards precancerous lesions, and invasion leading to malignancy .HPV genomic amplification always happen close to the epithelia differentiation programme and often induce hyperplasia of the epithelial cell, which manifest clinically as cervical intraepithelial neoplasia grade 1(CIN1)(Kukimoto, 2015). CIN2(moderate dysplasia) and CIN3(sever dysplasia) are the middle and the late stages respectively referring to the lesion happened in the lower two third and more than two third of the epithelium which are the