艾滋病毒 z-bo 2020-10-19 494

　　Although some HIV drugs can control infection well, they still cannot eliminate HIV. The reason is that the pharmaceutical ingredients of these tablets cannot reach the hidden reservoir of the virus lurking in the infected white blood cells. Scientists believe that uncovering the secret of this potential virus pool can not only control but also cure HIV.

　　MichelC from Rockefeller University. Researchers and collaborators led by Professor Nusenwijk have presented some new insights that reveal cells that may and are unlikely to hide this potential threat. Lillian Cohn, a graduate student at the Ussenzweig Institute of Molecular Immunology, said: “Recent research shows that white blood cells multiply over time and produce many clones. All clones contain the genetic code of HIV. It does not seem to contain a virus library. Our analysis It shows that certain cells are the source of potential virus reservoirs and have not undergone cell division."

　　HIV is a member of this family of retroviruses. After the initial infection, they can all be inserted directly into the genome of the host cell and hide quietly. The main target of HIV is CD4 T lymphocytes, a type of T cell involved in triggering an immune response.

　　When HIV is integrated into the genetic code of CD4 T cells, it will cause active infection, hijack the cell and produce copies of HIV that infect other cells, thereby killing the infected cell. .. Some antiretroviral drugs that prevent HIV infection work by interfering with this hijacking. However, these viruses may not cause active infections, and instead leave small, quiet DNA fragments in the host cell's genome. In this case, these drugs cannot be destroyed and the infection is still potential.

　　But what actually happens is often in the middle. HIV manages to allow at least part of the virus to enter the T cell genome, but some problems in this process prevent the virus from hijacking the cell and replicating itself. However, certain successful integrations can still cause damage, and the exhaustion of the immune system leaves patients still vulnerable to opportunistic infections that can be fatal years or decades after the initial infection.

　　Cohen said: "When patients stop taking antiretroviral drugs, the infection will return. Surprisingly, these viruses can cause AIDS 20 years after the initial infection."

　　To study a potential virus reservoir hidden in a type of CD4 T cell: a long-lived memory cell that can help the immune system remember specific pathogens. When these cells encounter a pathogen they have seen before, they stimulate the proliferation of T cells that recognize the pathogen. This process is called clonal propagation. Previous studies have shown that clonal expansion is very important for maintaining the HIV latent virus pool.

　　By following the work of Mira Jankovich, a senior researcher in the laboratory, Korn and his colleagues tested CD4 T cells and unique CD4 T cells cloned from blood samples of 13 HIV-infected people. Achieved using the analytical calculation technology developed by the experimental assistant researcher Israel Tojarda Silva (Israel Tojarda Silva) to determine the integration site where HIV inserts itself into a single cell.

　　Cohen said: "Given the huge human genome, it is impossible for HIV to insert multiple times at the exact same position. Therefore, viruses contained in multiple cells have the same integration site. If they are, they are classified as The same clone; if a cell contains a unique merging site, and the location is not shared with other cells, the cell is regarded as the only cell. 75 viruses obtained by the additional cell clones of the expansion test The sequence confirmed whether they could produce more viruses. However, I found that the sequence could not do this.

　　"We cannot rule out that rare cell clones may contain active viruses, but the most likely scenario is: potential virus storage and potential for treatment of HIV: therapeutic targets are in their own integration, which is rare in a single cell."