You ask an interesting question. Typically, the ability for ionizing radiation to cause a biological effect (such as clonogenic cell death) is based on Lea's Target Theory. Because the volume of a virus' critical target is so much smaller than that of a mammalian cell, viruses are significantly more radiation resistant. But, if I understand this question, you are asking about the usefulness of irradiating cancerous cells created (primarily) from an exposure to a virus. Here, the carcinoma will be significantly more radiation sensitive than its wild-type (normal) cell counterpart. Therefore, radiation therapy will work as before. That said, if the virus is present in the cells, there is (as with any virus located in the body) the potential that the radiation could cause the virus to mutate. This really isn't much of a concern since, for example, many people have a non-active version of the chickenpox virus in their body. If radiation were to cause an effect to that virus, we should see a statistically significant increase in the number of cases of shingles observed in irradiated populations.

You ask an interesting question. Typically, the ability for ionizing radiation to cause a biological effect (such as clonogenic cell death) is based on Lea's Target Theory. Because the volume of a virus' critical target is so much smaller than that of a mammalian cell, viruses are significantly more radiation resistant. But, if I understand this question, you are asking about the usefulness of irradiating cancerous cells created (primarily) from an exposure to a virus. Here, the carcinoma will be significantly more radiation sensitive than its wild-type (normal) cell counterpart. Therefore, radiation therapy will work as before. That said, if the virus is present in the cells, there is (as with any virus located in the body) the potential that the radiation could cause the virus to mutate. This really isn't much of a concern since, for example, many people have a non-active version of the chickenpox virus in their body. If radiation were to cause an effect to that virus, we should see a statistically significant increase in the number of cases of shingles observed in irradiated populations.

Thank you for your reply. Can the number of copies of the genetic material compensate for the pathogen treatment resistance?

Perhaps it is so that irradiation of the cells will affect the number of copies of the virus. A quantitative PCR of viral load before and after irradiation would therefore be a good decision. The amount would thereby be normalized to the amount of genomic DNA. A distinction between integrated and non-integrated viral DNA would also be helpful.

The radiotherapy for virus-associated tumors can not noly cause mutant cells death, but alse a local radio injury following inflammation and antigen exposure. It's helpful to clear pathogens--HPV. Here, antigen exposure can be either virus exposure or tissue damage or both (synergie of PAMPs & DAMPs). On the other hand, radiotherapy is a relative selective treatment comparing to other physiotherapy, such as frozentherapy. This is what I know the positive side.

I don't deny the possibility of virus mutation increasing the level of malignancy. Maybe the mutant virus promotes metastasis and recurrence, and even more, the spreading of virus in the population could cause more serious consequence. We need strong laboratory proof, and then thinking about strategies.

I'm still a student, and not sure for what I said.

When the tumor-associated virus is replication competent, ionizing radiation, in fact, may lead to an enhanced immune response. On the other hand, the fragmentation of the genomic DNA under the irradiation results in an increased probability of the integration of viral DNA into the host genome. This is to be mindful. Since there are different types of HPV, it would be a favorable constellation for another cellular transformation for carcinogenic types HPV 16 and HPV 18.

Your hypothesis has universal value. This pattern applies to many situations. But there are situations where the integrations induced by radiation perhaps make no sense. If integrations during natural pathogenic process are more significance than those caused by radiation in terms of efficiency and frequency. Before somatic cells morph into malignancies, there always been long term chronic infection and maybe countless virus integrations. The radiation is more harmful in the stages of infection and CIN, since the tumor has already produced, another carcinogenic process is redundant anyway.

The phenomenon of host cell reactivation after ionizing radiation is well known since more than 60 years. It was investigated in the 1960th. As such it is possible to kill virus-accociated cells by ionizing radiation, but ... virus particles may be liberated which (to small to be the target for killing by ionizing radiation) may cause virus-infection of non-irradiated somatic cells.

Very interesting discussion, I have been trying to find studies that report recurrence of cervical cancer after all the available treatment for this conditions. I am thinking that if the HPV are mutated and the mutant turn-out to be more oncogenic (if the mutation has any clinical value) and are not cleared with the radiation damaged cells, then we may expect to find more recurrence after radiotherapy than the other treatment of cervical cancer.

I will appreciate any reference or citation of any research report that may help my efforts. this may inform a more detailed laboratory based research/study

In the case of oropharyngeal tumours, those caused by HPVs respond far far better to chemo/radiotherapy than those caused by tobacco and alcohol, which respond best to surgery.