In Virus TaxonomyPublisher Summary This chapter focuses on the Herpesviridae family whose current members have hosts that include reptiles, birds, and mammals. The nucleotide sequences or predicted amino acid sequences of its subfamily Alphaherpesvirinae form a distinct lineage within the family. A region of the genome comprising the unique short sequence US and flanking internal and terminal inverted repeats IRS and TRS contains genes homologous to those found in HHV-1 and characteristic of the subfamily. The viruses productively infect fibroblasts in culture and epithelial cells in vivo and many of its members cause overt, usually vesicular epithelial lesions in their natural hosts.
Mitogens substances outside the cell which stimulate cell proliferation and growth factors usually act on cell surface receptors to activate signalling molecules which affect gene transcription leading to accelerated cell growth. Oncogene proteins are also present in the intracellular signalling from integrins surface proteins mediating cell motility, attachment and associated growth signals.
Whereas tumor suppressor gene mutations can be described as "faulty brakes", oncogenes can be characterized as "stuck accelerator pedal". Most growth factors act by binding to transmembrane tyrosine kinase receptors on the cell surface membrane.
From the point of view of cancer, the most notable cell signalling pathway is the one activated by the Ras protein attached to the inner cell surface associated with the tyrosine kinase receptor. Oncogenes of the Ras protein mutated proto-oncogenes cause Ras to be perpetually active, whether a growth factor is present or at the tyrosine kinase receptor or not.
Nearly a third of all human cancers have the ras oncogene, forming a defective Ras protein. Both the p53 tumor-suppressor gene and the ras oncogene promote VEGF secretion — promoting angiogenesis growth of new blood vessels required to support new, rapidly-growing cancer tissue.
Cell Receptor Signalling to the Nuclear Transcription Factors The transcription factor proteins Fos, Jun and Myc come from proto-oncogenes designated as immediate early genes because they are expressed rapidly after mitogen stimulation and have a short half-life.
The proteins from immediate early genes are transcription factors produced in response to cell stimuli, and these transcription factors cause the production of functional proteins. Oncogenes produced mutated forms of the immediate early genes which can increase the activity of the proteins they form.
Overexpression of the Myc growth factor can lead to the angiogenesis and tumor-cell invasiveness that characterizes malignancy.
Myc overexpression increases Bcl2 protein and decreases p53 protein, both effects being anti-apoptotic and pro-proliferative.
Myc DNA targets are often tumor-suppressor genes that are frequently silenced by methylation in cancer. The ability of G-protein-coupled signaling pathways to undergo desensitization to receptor substances "tolerance" is part of the basis for addiction to opiates, caffeine, benzodiazepines and nicotine.
Thus, PTEN mutations which make the protein defective release two pathways which can lead to excess proliferation and thus to cancer. Neutrophils and macrophages immune system cells enter the wound and fight bacteria by creating toxic free radicals like hydrogen peroxide, peroxynitrite and the hydroxyl radical.
Antioxidant enzymes like selenium-containing glutathione peroxidase and thioredoxin reductase protect neutrophils, macrophages and other tissues from the free radicals intended to destroy pathogens. Macrophages release growth factors to promote tissue re-growth.
Continuous exposure to the free radical peroxynitrite leads to DNA mutation. Growth factors from macrophages promote proliferation of new cancer cells. Non-infectious causes of chronic inflammation such as tobacco smoke and asbestos also contribute significantly to cancer.
Although the main carcinogenic effects of inflammation are on tumor promotion and progression, chronic inflammation can also lead to tumor initiation.
Septic shock is the main cause of multiple organ system failure, the leading cause of mortality in intensive care units. During infection DNA damage in pathogens is beneficial, but in chronic inflammation the body's own cells become the victims.
The hyperproliferation associated with chronic inflammation leads not only to decreased genome stability and increased mutation, but to hypermethylation see Section F. There are also great differences in susceptibility to cancer between different organs and tissues, not all of which can be attributed to environmental differences.
Cancer results from DNA changes that re-direct cellular activity away from anything other than reproduction, growth and invasion of other tissues. Although cancer is a disease of DNA mutation, the vast majority of those mutations are acquired due to environmental influences especially chemical rather than by heredity.OPGELET.
Patienten en leken die raadgevingen/adviezen/informatie zoeken via deze verzameling links wordt dringend geadviseerd de verzamelde informatie te bespreken. Abortion is the ending of pregnancy due to removing an embryo or fetus before it can survive outside the uterus.
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Human herpesvirus infections are endemic and sexual contact is a significant method of transmission for several including both herpes simplex virus 1 and 2 (HSV-1, HSV-2), also human cytomegalovirus (HHV-5) and likely Karposi's sarcoma herpesvirus (HHV-8).
Overview of the Human Herpesvirus 1 Essay - The Human Herpesvirus 1 is a member of the Herpesviridae family and belongs to the genus virus. The origin of the word “herpes” comes from the Greek meaning “to creep”.
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The Human Herpesvirus 1 is a member of the Herpesviridae family and belongs to the genus virus. The origin of the word “herpes” comes from the Greek meaning “to creep”.
This is such a fitting description for a virus that causes sores which creep and spread across the skin of an infected.