Viruses are mainly known to cause diseases, but a study recently characterized by the Harvard Medical School identifies a kind of virus that could be more “friend” than “enemy”. In a provocative attitude, Harvard scientist suggests that the human beta -papillomavirus could protect us from skin cancer instead of causing it.1
When the sun is shining, we are pulled outwards. The sun increases our mood, energies us and gives some of us the beautiful summer lights, but while taking on rays, too, too much sunlight can be harmful to our body and our minds. UV radiation damages our skin cells and means that they age faster and, in the worst case, turn into cancer cells. While careful sunlight and proper protection can reduce the risk of skin cancer, scientists have found that we may receive additional help from an unexpected ally: viruses.
Beta papilloma viruses are less pathogen than other members of the Papilloma family family. In our skin cells that live quietly, they occasionally cause Verruca or may trigger psoriasis. In contrast to their cousins of the apartment in the mucous membrane, Alpha HPV, they do not trigger cancer or outbreaks from warts. Scientists recently discovered that they can help our immune cells to see when epithelial cells are at risk of becoming cancer -like.
The way in which sunlight can damage our skin cells and lead to skin cancer are well examined2. Ultra violet radiation violates DNA in our skin cells, which impair the functions of the cells and progresses to cancer. Of course, the body has a means of preventing this fate; For example, it can repair the DNA damage. If the damage is outside the repair, the cell runs out a suicide program before the damage gets out of control and can develop into cancer.
P53is one of the most important “tumor -uppressor” genes that need to be identified. The P53 protein plays an important role in the cellular reactions on DNA damage. If the DNA is injured, P53 can either ensure timely DNA repair or cell death. If the gene that codes the P53 itself, is affected and the protein does not work as intended, the cell unfortunately becomes susceptible to cancer -related changes. In the laboratory, when a scientist switches the P53 gene in a cell, they also replicate in situations in which they should not – just like in cancer cells.
This tumor that prevents protein is essential to combat cancer -in up to 90% of the second most common skin cancer -cutan squamous crew carcinoma, doctors find that the patient has a faulty P53 gene.
Viruses generally have a bad reputation because they can cause some of the worst illnesses known to humanity. So it could surprise you that some viruses can help us to fight against the disease and to extend our lives.
In a paper published at the beginning of this year Cancer cellThe Harvard Medical School investigators, a prestigious research journal, suggested that the beta -papillomavirus (beta hpv) could prevent skin cancer. This is correct, this viral avant -garde alerts the body’s immune system to eliminate the cells damaged by UV radiation before they become cancer -like.
How could a common skin virus help our immune cells to recognize signs of UV damage?
Historically speaking, pathologists and cell biologists have found that human papillomavirus viruses of Beta have often occurred in skin cancer lesions. First of all, cancer doctors wondered whether the Beta -HPV infection such as Alpha HPV in the mouth or cervix changed, which triggered cancer -like changes in the cells. In 2019, however, the cancer researchers found that hairless mice that were infected with the virus Less likely Develop skin cancer.4 This 20251 Study browses deeper into these results and asks the question: What is going on in the cells?
The team started returning to these mysterious mice. What caused the protective effect?
Even after extensive UV exposure, mice are susceptible to skin cancer, and just like in humans, a mutation of his P53 protein sets the skin cells on a way of becoming cancer. The researchers infected half of the mice with the mouse version of the beta papillomavirus and then blew infected mice and their non -infected brothers and sisters with daily doses UV radiation. They used a special type of hairless mouse for two reasons; First, it makes it easier for us to see when the mouse develops a lesion, and secondly, Mausfell blocks UV radiation. This saves a lot of time for shaving if you don’t have a bald intervention!
After several months of synthetic sunburn, the mice developed skin lesions that showed signs of early skin cancer – a missing or incorrect P53. If the team compared the precancer cells from Beta -MPV mice with non -infected mice, they found an important molecular false adjustment.
The researchers found that the mice infected with the virus had much smaller preliminary core lesions than their infected siblings. Just like in nature, incorrect or missing P53 Croon Control proteins caused precancator. When the team infected a different set of mice with another skin virus, it did not see the same effect – all mice had precancatorous lesions of a similar size, and everyone was missing or incorrect P53. This in particular signals something special about the Beta -MPV that the cells that P53 lacked no longer multiply.
When the researchers look at a closer look at the differences between the virus -infected precancator and near cells, they found that if they had malfunctioning P53, they contained much higher amounts of papillomavirus as cells with a normal version of P53.
When the researchers examined the two immune response of the mice, they found that the preceded skin areas infected with virus attracted immune cells faster and more effectively than skin lesions in which no beta -MPV contained them. The immune cells killed the damaged skin cells before they could become cancer -like.
In short, they found that the virus, if they infected a mouse with Beta -MPV, failed as UV damage in P53. As soon as the Beta -MPV infection had reached a certain level, the SOS signals cell triggered the immune system. Cell kits white blood cells answered the call, with the cells infected with the virus. Fortunately for the mouse, the virus destroyed the precancer cells and prevent the tumor from growing.
If P53’s damage limitation fails, the papillomavirus occurs and alarmed the immune system.
After discovering this immunogenic effect in mice, the next step was of course to see if it works in humans3.
The skin cancer scientists collected skin samples from faces and torsos of the people. Since our faces receive more sunlight, they found more signs of UV damage there during inspection. Interestingly, the sun-delayed facial skin had more beta-human papilloma virus compared to the skin from the upper body. And here is another turn: Precancerous skin spots actually had less beta -hpv than the surrounding skin. It seems as if these patches became cancer -like because they didn’t have enough beta -hpv to call up the immune system for the backup.
The research of the relationship between human skin cells and beta papillomavirus is still in its infancy. The exact molecular mechanism of this “viral sunscreen” is not completely clear.
However, these results show that viruses are not always bad guys – they can be unexpected allies. Since scientists continue to examine this fascinating relationship between us and viruses, we could find that they are more than just pests. Some of them could be tiny, unsung heroes that help us stay healthy.
References:
1: Son Hg, Ha Dt, Xia Y, Li T, Blandin J, Oka T, Azin M, Conrad Dn, Zho, Zeng Y, Hasegawa T, Strickley JD, Messerschmidt Jl, Guennoun R, Erlich Th, Shoemaker GL, Johnson LH, Palmer Ke, Fisher de, Horn, Nazarian RM, Joh JJ, Demehri S. Come Salpapillomavirus immunity preserves the homeostasis of highly mutated normal skin. Cancer cell. 2024 Dec 7: S1535-6108 (24) 00448-3. DOI: 10.1016/J.CCELL.2024.11.013
2: Carvalho C, Silva R, Melo Tmvdpe, Inga A, Saraiva L. P53 and the ultraviolet radiation -induced skin reaction: Find light in the darkness of the triggered carcinogenesis. Types of cancer. 2024; 16 (23): 3978. Https://doi.org/10.3390/cancers16233978
3: Offord C. The common virus can help protect the skin from sun damage. 2024 Dec 12. Virus can help protect the skin from sun damage | Science | Aaas
4. Strickley JD, Messerschmidt JL, Awad Me, et al. The immunity against coming salpapilloma virus protects against skin cancer. Nature. 2019; 575 (7783): 519–522. Two: 10.1038/S41586-019-1719-9