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Papillomavirus silences innate immune response

Date:
December 7, 2009
Source:
Helmholtz Association of German Research Centres
Summary:
Human papillomavirus type 16, the most common cause of cervical cancer, silences a key signaling molecule of immune response in its host cells. Once the body's own immune defense is missing, the pathogens are able to infect the cells of the cervical mucosa even more successfully. Scientists have found out that the viral E6 oncogene is responsible for this mechanism.

Scientists have discovered a mechanism by which the E6 oncoprotein of high-risk HPV16 promotes carcinogenesis.
Credit: Image courtesy of Helmholtz Association of German Research Centres

In the 1980s, Harald zur Hausen and his co-workers discovered that specific types of human papillomavirus (HPV) cause cervical cancer. Scientists soon found out how these pathogens cause cells to degenerate. It is known today that the main culprits are viral proteins E6 and E7. Both proteins switch off different cellular control functions, thus promoting cell growth.

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Professor Dr. Frank Rösl and his co-workers at DKFZ have now discovered another mechanism by which the E6 oncoprotein of high-risk HPV16 promotes carcinogenesis. The oncogene silences production of an immune protein called interferon-kappa. Interferons are proteins which are part of our immune system and are responsible primarily for stimulating the immune response to viruses and tumors. Interferons are produced by white blood cells and other cell types. Interferon-kappa is relevant for HPV infections, because it is produced mainly in cells of the skin and mucosa (keratinocytes) which are the preferred hosts of the viruses. If interferon-kappa is not working in cells, other proteins involved in immune defense also cease to function properly.

Dr. Bladimiro Rincon-Orozco of Rösl's team has now shown for the first time that HPV16 switches off the interferon-kappa gene by biochemical modification of DNA. Such alterations of the genetic material are called epigenetic mutations. Studying HPV infected cells in a culture dish, the research team observed that interferon-kappa is epigenetically silenced. They were later able to confirm this result in cervical cancer tissue samples.

"Interferon-kappa is an important part of what is called innate immunity," Frank Rösl explains. Using this evolutionary old defense mechanism, the body can defend itself immediately after being infected with pathogenic agents, while formation of the specific "acquired" immune system may take some time. "By switching off the interferon production, the viruses prevent infected cells from being destroyed by this type of immune response," says Rösl, explaining the strategy of the virus that causes cancer. In the next step, the researchers are planning to investigate whether administering interferon-kappa can slow down the growth of cervical cancer cells and may thus support treatment of the disease.


Story Source:

The above story is based on materials provided by Helmholtz Association of German Research Centres. Note: Materials may be edited for content and length.


Journal Reference:

  1. Bladimiro Rincon-Orozco, Gordana Halec, Simone Rosenberger, Dorothea Muschik, Ingo Nindl, Anastasia Bachmann, Tina Maria Ritter, Bolormaa Dondog, Regina Ly, Franz X. Bosch, Rainer Zawatzky und Frank Rösl:. Epigenetic Silencing of Interferon-%u03BA in Human Papillomavirus Type 16-Positive Cells. Cancer Res, 2009; 69: (22) November 15, 2009

Cite This Page:

Helmholtz Association of German Research Centres. "Papillomavirus silences innate immune response." ScienceDaily. ScienceDaily, 7 December 2009. <www.sciencedaily.com/releases/2009/12/091203112155.htm>.
Helmholtz Association of German Research Centres. (2009, December 7). Papillomavirus silences innate immune response. ScienceDaily. Retrieved December 22, 2014 from www.sciencedaily.com/releases/2009/12/091203112155.htm
Helmholtz Association of German Research Centres. "Papillomavirus silences innate immune response." ScienceDaily. www.sciencedaily.com/releases/2009/12/091203112155.htm (accessed December 22, 2014).

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