The Viruses: What Keeps Them There
The viruses are oncogenic virus has the ability to make the cell cancerous quila infect
. The word "oncogene" is derived from the Greek oncos, which means "tumor".
In general, they are responsible for 15% of cancers. These viruses have generally the same characteristics as other viruses (Daction mode, structure, composition) and have the option infection is both Lhomme than others species (animal or vegetable). For the tumor nature occur, the virus must enter into an abortive cycle and sintegre the cellular genome, which is not systematic, as it can go into the lytic cycle and cause cell lysis.
These viruses are classified into five categories:
- Herpesvirus (DNA), eg, Epstein-Barr virus (cancer of the pharynx, nose)
- Adenovirus (DNA), eg, adenovirus type 12 (cancer of the respiratory tract, gastrointestinal tract)
- Papovavirus (DNA), eg, human papillomavirus, SV40 (cancer of the cervix ...)
- Hepadnavirus (DNA), eg Hepatitis B (liver carcinoma)
-Retrovirus (RNA), eg: ALV (Avian Virus Leukos) (avian leukemia)
Like all viruses, their genomes have multiple structural possibilities, however, we can distinguish two main mechanisms by infection is general support linformation genetic DNA or RNA.
The DNA present oncoviruses oncogene gene in their genome and are able to lexprimer sintegrant partially or completely and randomly into the genome of infected cells. The products of this gene are oncogenic alter the development of normal cell and transform it. Such products may be involved in replication, be transcriptional repressors, bind to an other cell proteins
During the abortive cycle, the virus accelerates the input of the cell in S phase which enables it to replicate more quickly because the nucleotide metabolism is amplified. In normal cell cycle is controlled by the G1 pRb protein that forms a complex with E2F and blocks Lexpress of cell cycle genes. Indeed, E2F is bound to Ladner with DP1 (transcription factor) and between them induce the expression of cyclin E and A necessary for the transition phase S. A second check takes place at the level of p53 protein that prevents phosphorylation of pRb thus remaining bound to E2F. Furthermore, the combination of induction of the expression of p53 and E2F tend to induce apoptosis.
That is therefore on these two proteins will act where the translation products of oncogenes (early proteins). Example: in the case of the transforming factor is SV40 T lantigene alone dimmortaliser and can transform cells by binding pRb and p53. For persistent or abortive infection has Quil there must have continuous expression of these factors transformants. Depending on the viral factors are different but lon is some convergent evolution.
Oncogenic RNA viruses are known oncornavirus, they are part of the family of retroviruses. They have properties in common outside on the envelope that is derived from the plasma membrane and studded with glycoprotein spikes (functioning as a membrane glycoprotein receptor) but also their core contains a helical nucleoprotein with an organization, their genome is diploid with two DARN stranded molecules identical in many ways connected by hydrogen bonds. Each of these molecules contains all linformation required for replication of the virus including three genes that are essential to the replication:
- Gag gene (code for proteins of the nucleocapsid)
- The pol gene (encodes the reverse transcriptase)
- The env gene (encodes the viral proteins on the envelope)
Some viruses have an additional gene is a gene oncogene. Replication of oncornavirus is very special, it passes through the reverse transcriptase by making copies dADN stranded dune and by synthesis of complementary strand and then power is integrated in the host genome by an integrase. Subsequently, the mechanism of cell transformation will be similar to that of DNA viruses.
by: Barbara Herbert
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