Porcine Parvovirus Essay

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).

I’m pretty sure that once in your life you have heard the word or term “Parvovirus”, or in its shortened form, “Parvo”. Likely, if you have heard of this word you know it isn’t a great one. Canine Parvovirus is a severe life threatening virus, hence the name, found in dogs of nearly any size and usually found in dogs 6 months or younger. The Parvovirus attacks blood cells and sharply affects the intestines. In 1967 the parvovirus was discovered and given the name CPV-1 and at the later period of 1978 a new kind of Parvovirus was discovered and called CPV-2. CPV-2 is the main form of the Parvovirus that is still seen today. Other varying animals that Parvo is found in are coyotes, foxes, and wolves. In this essay I will discuss how Parvo is contracted, the symptoms of Parvo, how you the owner can help your dog if symptoms are shown, how to avoid your dog contracting the Parvovirus, and how it is treated.

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

Papillomavirus has to get inside a cell to cause disease and virus mimics the cell cycle of the host cell to optimize conditions for more efficient viral genome replication. Research suggest that the HPV virus enters the human body via a micro tear on

Nakano et al., 2003; Tadagaki et al., 2005; de Munnik et al., 2015; Montaner et al., 2013

The early viral genes E6 and E7 can influence both replication and transcription of the virus, and also interacts with host regulatory proteins [2]. Upon infection of the host, the viral genome ring is disrupted leading to its ability to incorporate its genome into that of the host's [2]. Once the viral early proteins interact with the host’s regulatory proteins, the host cells will lose function of regulating tumor suppression, ultimately stimulating the proliferation of the HPV infected cells [2][7]. Papillomaviruses tend to replicate within cells through the lysogenic pathway, and incorporate its viral genome into the host’s genome [7]. Stated earlier, early detection of this particular virus is challenging because the

Human papillomavirus (HPV) infections cause cervical cancers, and some cancers of the vulva, vagina, penis, anus, and oropharynx. Two prophylactic HPV vaccines (Gardasil® and Cervarix®) can block new infections from a subset of the most prevalent HPV types, but have shown no therapeutic effect against pre-existing diseases. No effective therapeutics exists at present, and the mechanisms of HPV-associated disease progression and cancer are not well understood.

On the other hand, hyper activation of IRE1 can affect c-Jun NH2-termina kinase (JNK), Nfkβ and the process known as IRE1 dependent decay (RIDD), which has ability to decrease some mRNAs, microRNA (miRNAs), including (miR-17, miR-34a, miR-125b,and miR-96) (46) to reduce more loading of ER

Wounding has been reported necessary for a HPV pseudovirus to deliver marker gene in mouse vaginal tract (Roberts et al., 2007). For skin infection, we found that pre-wounding did improve the viral infectivity in our rabbit papillomavirus model (Cladel et al., 2008). We compared vaginal infection with and without wounding in our MmuPV1 model. Although we found that wounding promoted infection at an earlier time, but it is not essential for MmuPV1 infection at the genital tract. One reason is the nature of low amount of target DNA encapsidating inside pseudovirus (Holmgren et al., 2005). Our unpublished study demonstrated that natural virions contain most viral DNA. Therefore, the efficiency of naturally viral infection is much higher when compared with the

Parvovirus is a relatively new disease that appeared in the late 1970s. It was first recognized in 1978 and spread worldwide in a few years. The virus is similar to feline panleukopenia (a feline version of Canine Parvovirus); they are 98% identical, differing in only two amino acids in the capsid protein VP2. It is also highly similar to mink enteritis, and the parvoviruses of raccoons and foxes.[4] It is possible that Parvo is a mutant of an unidentified parvovirus of some wild carnivore. Parvo does not cause disease in cats and does so only mildly in mink and raccoons but is almost entirely affecting canines.

Gardasil contains VLPs of HPV16, HPV18, HPV6 and HPV11 that are produced in yeast (5). Both Cervarix and Gardasil target oncogenic HPV types, but Gardasil, with addition of VLPs of HPV6 and HPV11, also target the risk of genital warts. (8). The newest vaccine, Gardasil 9 was approved by FDA in 2014. It protects the vaccine receivers against an even wider range of HPV types including HPV 6, 11, 16, 18, 31, 33, 45, 52, and 58 (1). Since the vaccines are only made from capsid protein without involving any live, killed virus or even viral DNA, these vaccines cannot cause any HPV-related illness and therefore very safe. In the other hand, L1 capsid protein is a strong immunogen that induces the development of neutralizing antibodies. In addition, aluminum salt adjuvant is used in both vaccine formulas to precipitate and ensure slow release of the HPV antigen in order to enhance antibody responses (5). The combination of all these components creates very safe yet effective vaccines against HPV.

Clearly, the development of cell culture systems for the newer HPyVs is important, in order to advance research into their biology, for example, the possibility of isolating and growing the infectious polyomavirus particles in the laboratory or experimental system.

Any threats that can be resolved by a healthy individual might become problematic for these patients. The blood safety becomes a major concern to protect them from catching diseases from the blood products. In our preliminary studies, we have demonstrated that intravenous infections via ear vein with papillomavirus induced tumor growth at locally wounded skin, anogenital, and oral mucosal sites in these two preclinical models. Transfusion with virus contaminated blood also induced tumors at locally wounded sites. To further delineate the risk of blood born papillomavirus and the viral DNA, we plan to determine the threshold dose with a serial of virus and viral DNA dilutions. Both immunocompetent and compromised animals of different ages will be tested in the current study to determine whether different threshold doses for infection by the circulating virus exist. Viral presence will be tracked with our established virological assays. Serum samples will be collected to monitor antibody generation.

Arraystar mouse circRNA Microarray (8×15 K, Arraystar) was adopted to detect circRNA expression, and 238 circRNAs were detected.