Viruses are usually supposed to worry us, but this is not the case with inoculate viruses. those that infect cancer cells and kill them, ignoring healthy cells.

So it is no wonder that the search for such viruses attracts many researchers.





What is the connection between viruses and cancer? What is the connection between viruses and cancer?

The Seneca Valley virus.

This virus also known as Senecavirus affects pigs and cows. In recent years it has been found that the virus attacks human cancer cells.



The ability to identify tumors and ignore normal cells tested in two trials. The first in relapsed solid tumors in children and the second in lung carcinoma.



Experiments also found that the immune system was removing the virus from the body. Thus preventing it from completing its anticancer action.

Ongoing research to understand how the Seneca Valley virus may be used for cancer treatments.

Researchers at the University of Otago in New Zealand discovered in 2017. That the virus binds to a receptor called ANTXR1, which is active in more than 60 percent of the cancers in humans.

ANTXR1, or its full name 'Anthrax Toxin Receptor 1' is a receptor that binds to the toxin molecules. This molecules released by Bacillus anthracis are the cause of Anthrax.



Turns out that this receptor appears mainly in human cancer cells. Its second version ANTXR2 appears in healthy body cells.

New study published in the PNAS journal. Researchers have been able to understand how this virus associate with the 'sick' receptor.



They used a cryogenic electron microscope to see the link between them at a resolution of only a few atoms.



The researchers compared the structure of the two receptors. Trying to understand which part of the ANTXR1 receptor allows it to bind to the virus.



Taking 7,000 pictures, Researchers discovered amino acids. Those acids link the receptor to the virus. Which differentiates between the two receptors.

The relationship between viruses and cancer. "To vaccinate the virus" The new discovery allows us to understand how the immune system identifies the virus.



The virus uses area to bind to the receptor converges with the region of the virus that the immune system antibodies identify and bind to. The immune system antibodies identify the virus. This helps researchers make changes to the structure. So that it can continue its anticancer activity without the body fighting it.



Such a move may be dangerous as it will improve the virus's ability to destroy cancer cells. But also produce a virus that is resistant to the immune system.



A possibility is the to suppress the immune system when treating the virus. But such treatment harm the ability to attack cancer with the help of the immune system.



As is currently done in immunotherapy and cancer vaccines, which aided by the natural ability to identify tumors and destroy them. Researchers need to combine creativity and discretion to develop the next drug that will end cancer.



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The Seneca Valley Virus in Close To Nuclear Resolution. The structure demonstrates how the virus binds to its cellular receptor. The Anthrax toxin receptor. Type 1 of this particular receptor is selectively expressed in as much as 60% of human cancer cells. As well as enables the virus to infect and demolish them though not impacting healthy cells.



Research study published in the journal Proceedings of the National Academy of Sciences, USA. Show how the virus is able to identify its target and leave regular cells on its own.



OIST Scientists Utilized cryo electron microscopy to rebuild the Seneca Valley virus structure.





Viruses engineered to attack malignant cells act as a cancer cure in some cancer patients.



Cure cancer with a virus. Credit: GUYCO In 1904, a woman in Italy experienced two life-threatening events: a diagnosis of cervical cancer and a dog bite.

Because of the bite, doctors gave her a rabies vaccine vaccine after which the huge tumor disappeared and the woman lived without cancer until 1912.

Immediately, several other women who had cervical cancer received the vaccine containing rabies and weakened rabies.

In 1910, reported that some of the patients had contracted the tumors, probably because the virus had killed the cancer cells in some way.



Genital HPV infections are ubiquitous. Cofactors which customize managing host cell genes are most likely to determine the different geographical rates of cervical cancer incidence.





A host cell-mediated intracellular control down-regulating particular HPV genes (E6, E7) in replicating healthy cells appear to be disrupted in cancer cells. Due to structural adjustments of the specific host cell genes obtained in the course of HPV DNA persistence. Infections with specific kinds of human papillomaviruses (HPV) have emerged as needed but not sufficient aspects for the development, at least, of the majority of cervical, vulvar, penile, and perianal cancers.









