Food and Drug Administration. This meeting of the Vaccines and Related Biological Products Advisory Committee VRBPAC is being held to discuss the use of cell lines derived from human tumors as substrates for the production of preventive viral vaccines. Corporate Authors. Publication Date. Page Count.
Source Agency. Document Type. The incidence of MCC has tripled over the past two decades, and the concern for MCC grows as the aging population with prolonged sun exposure increases. This chapter summarizes recent discoveries in MCPyV molecular virology, host cellular tropism, cell culture infection and animal models, and the unique genetic features of MCPyV that make it the only polyomavirus discovered to date that is associated with a human cancer. MCPyV is more likely to induce MCC in immunocompromised patients, thus providing an excellent probe for examining the role of the host immune system in controlling virus-induced oncogenesis.
The interplay between MCPyV infection and host immune response and how disruption of this virus-host interaction may contribute to MCC pathogenesis is also reviewed. Together, our current knowledge provides a platform for future mechanistic studies to fully elucidate the MCPyV infectious life cycle and the mechanisms by which MCPyV infection contributes to MCC pathogenesis.
To do so, viruses interface with a number of cellular processes including the host DNA damage response. DNA viruses have a particularly precarious situation, in that they must infect cells without alerting the host DNA damage response pathway to recognize and launch a response against the viral DNA genome. This challenge has required DNA viruses to develop unique methods to allow the virus to interact with and evade the host DNA damage response. These viruses modulate the DNA damage response by activating or deactivating sensors of DNA damage as well as key downstream effector molecules.
Here we review the current literature discussing the integrated relationship between DNA tumour viruses and the host DNA damage response during lytic and latent viral infection. Javier Pages: Shortly thereafter, this human pathogen was additionally shown to have the capacity to induce malignant tumours when inoculated into experimental animals. By representing the first known tumourigenic human virus, adenovirus attracted many talented scientists to study its oncogenic properties.
The resulting work demonstrated that adenovirus is a powerful tool for exposing general molecular mechanisms that commonly trigger the development of cancers.
Another advancement stemming from these investigations was the adenovirus vector, which arose from technologies that allowed manipulation of the adenovirus genome and production of cell lines that stably express adenovirus genes.
Considering the tumourigenic properties of human adenovirus, it may be somewhat surprising that adenovirus vectors are now employed to combat human cancers. The goal of this chapter is to review the molecular mechanisms discovered for the adenovirus oncogenes and the promise of adenovirus vectors as effective cancer therapeutics. How to buy this book. EAN: Subjects: [medical microbiology] [molecular microbiology] [virology].
Books Site Journal Backlist Gateway. Issues Mol. How to Order. Library recommendation email pdf. Download flyer. Foreword Sally Roberts. Infections with certain infectious agents viruses, bacteria, and parasites have been identified as strong risk factors for specific cancers.
Numerous studies in humans, animals, and mechanistic evidences support a strong causal relationship between exposure to these four viruses and human cancer in at least one site, sometimes in several sites. Together, DNA viruses have been estimated to be responsible for 1. Merkel cell virus, another DNA virus, was discovered more recently in a rare skin cancer in human, and was classified as probably -but not definitively- carcinogenic to human by IARC in despite strong mechanistic evidence, due to the lack of prospective studies in human yet available.
In this chapter we give an overview of the burden of cancers attributable to DNA viruses in the world and in eight geographical regions. Then we summarize for each infectious agent and cancer site, the body of epidemiological evidence supporting our estimates of the attributable fractions. Biology of the Human Papillomavirus Life Cycle. Human papillomaviruses HPV are small, double-stranded DNA viruses that replicate in squamous epithelium and cause hyperproliferative lesions, some of which are at risk of malignant transformation.
The infectious HPV replication cycle is intimately linked to the differentiation program of this tissue. The virus infects undifferentiated basal keratinocytes to establish and maintain replication of the viral genome, whereas productive viral DNA amplification and formation of new progeny is restricted to differentiating keratinocytes.
Successful viral replication in differentiated cells requires the virus to reprogram the post-mitotic keratinocytes in order to support viral genome replication. The use of animal PV models and cell-based tissue culture models of the virus life cycle, combined with generation of recombinant virions for infection studies, has revealed much about the complexities of the HPV life cycle.
Defining the nature of the keratinocyte that HPV targets, infection strategies, and virus-host interactions necessary for virus DNA replication and virion production has contributed to the design of anti-HPV vaccines and the understanding of HPV-driven cancer development. This chapter aims to provide an overview of key HPV life cycle events and the models used to interrogate virus-host interplay.
They can infect the epithelia of the genital and upper respiratory tracts and the skin and are classified into several genera based on their DNA sequence.
A small number belonging to genus alpha, referred to as mucosal high-risk HR HPV types, are clearly associated with human carcinogenesis. A vast number of studies have demonstrated that the products of two early genes, E6 and E7, play a key role in cellular transformation and cancer development.
Both oncoproteins are very small molecules and do not have any enzymatic activities, but exert their biological properties by interacting with a large number of cellular proteins. These interactions result in modification of the activities of the cellular proteins, which, in some cases, are targeted to degradation via the proteasome pathway.
Inactivation of these key tumour suppressors strongly alters cellular gene expression, leading to chromosomal instability and cellular transformation. Epstein-Barr Virus and the Pathogenesis of Lymphoma. Burkitt lymphoma BL , first recognized by Denis Burkitt in , is a high grade B cell malignancy particularly prevalent in young boys in tropical Africa and New Guinea.
Epstein-Barr Virus and Epithelial Carcinogenesis. When viruses infect human cells, they must successfully resist host defences to faithfully replicate their genetic material.
Human adenoviruses were discovered through their ability to cause acute respiratory infections in people.
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