Nicola Staff asked 3 weeks ago
You are correctly seeing there are multiple reasons why such an analysis might fall short of finding every possible viral culprit responsible for creation of malignancies in the tumor databases examined. First of all, we have already stated that only 85% of cancers are viral in origin. Thus, there will be a significant number of tumors devoid of harmful viruses because they were caused by chemical carcinogens or random mutations occurring from radiation, etc. Secondly, once there is a flareup in viral infestation and sufficient arousal of the immune system in particular, as an aggravating factor in triggering malignant transformation because of damage to DNA, the cells will be under various kinds of stressful fluctuations and this might work against viral replication, even as the malignant cells begin propagating on their own, because they have become defective with respect to checkpoints that normally limit the number of divisions that can happen. There can also be some immune system control exerted during the initial surge of recognition of the presence of a malignancy, and that might work more effectively to reduce the number of viral particles than to actually kill malignant cells in some cases, and that could lead to an imbalance in the ratio of virus to malignant cells containing them. And as you rightly point out, not all carcinogenic viruses have been identified and have known sequences, so there are many tumors that will not be picked up in a search to match known viral gene sequences. But even as far as it goes, the data are quite heavily in support of what we have told you, that the majority of malignancy (85%) is virally caused and the traces will be present if only in low quantities and perhaps dismissed as artifacts when they are actually meaningful, just not glaringly obvious from being present in massive amounts. As you have described, once cells become malignant, they no longer need a viral presence to keep them going. So even with the open questions still being mulled over by scientists regarding the data from this exercise, the authors rightly point out there is quite a high frequency of viruses in both normal and malignant tissues raising questions here and no good way at present to know if there is a meaningful cut-off in excluding active participation in malignant transformation as a historical fact. So, we see this exercise as meaningful evidence in support of what we have told you about the quite common role of pathogenic viruses triggering malignancy.
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