the HTLV-1 virus can cause a cancer rare in some people. He enters a lymphocyte T and stay there. At first, it does not release any new virus particles and does not cause no harmful effect. Moreover, this state preserves itself indefinitely for the majority of the population. However, at nearly 5% of infected, the virus eventually activates decades after infection and modifies the operation T lymphocytes.
Rare cancer is called adult T cell leukemia / lymphoma (or ATL in English). In fact, HTLV-1 changes T cells by leukemia cells once it is activated. The time lag between infection and virus activation made it difficult to determine the how the modification occurs.
A international team led byImperial College London and theKumamoto University in Japan conducted research on the subject. The results of the work were published in The Journal of Clinical Ingestigation Wednesday December 15, 2021.
A transformation of T lymphocytes induced by the HTVL-1 virus
For their research, the international team analyzed more than 87,000 T lymphocytes. They come from healthy donors, from healthy carriers the HTLV-1 virus as well as patients with ATL. Scientists have sequenced the RNA of these cells and discovered how the virus interacts with T cells.
Once the virus HTVL-1 enabled, the researchers claimed that it makes the T lymphocytes infected highly active and over-reactive. In this state, they produce proteins that keep proliferating. At the same time, these same proteins help rebel cells to evade the rest of the immune system still healthy which in normal times would eliminate them.
Scientists believe that these changes make rebellious T lymphocytes plus sensitive to DNA damage. As a result, exposure to chemical agents or some radiations, for example, would accelerate the evolution to the cancer.
Hope to be able to prevent this type of blood cancer
the Dr. Masahiro Ono asserts that understanding the mechanisms behind this change is important. He believes that this discovery opens up new perspectives to researchers. In other words, it allows them to look for ways to interfere with this transformation. So they can hope to block evolution from disease to cancer. Note that Masahiro Ono comes from the Life Sciences Department at Imperial College.
“For example, chronic activation of T cells could be stopped by molecules that block signaling pathways that tell cells to activate. Alternatively, the treatments could target the proteins that activated T cells create to help them proliferate. “
Dr. Masahiro Ono
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