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Oct 8, 2020 /--- A new study published in eLife shows that HIV-infected cells that can identify HIV-infected people (PLWH) who receive antiretroviral therapy (ART) remain active for years.
results also showed that most of these immune cells (CD8 plus T cells) have the ability to interrupt hiv-1-infected cells that cause HIV-1 to rebound after treatment.
this insight can help develop new treatment strategies for HIV infection.
ART has transformed HIV-1 from a deadly disease to a controlled chronic disease.
, however, an infected person must take it for life, as interruption of treatment usually allows the virus to bounce back within a few weeks.
this rebound is caused by cells carrying HIV-1 DNA integrated into the human genome.
(Photo source: www.pixabay.com) "Although more than 95 percent of the original virus DNA cannot replicate and reactivate HIV-1, the rest of the "HIV-1 reservoir" we defined in our study maintains its ability to produce infectious virus particles and cause virus rebounds," explains Joanna Warren, a postdoctoral researcher in the Department of Microbiology and Immunology at the University of North Carolina at Chapel Hill.
" largest and most typical HIV-1 repository is located in 'static' CD4-T cells that circulate in the blood and live longer.
" has two strategies that allow people living with HIV-1 to stop ART treatment without a virus rebound.
both methods can use HIV-1-specific CD8 plus T cells to reduce or eliminate THE-1 library.
However, mutations (or mutations) in viral particles present in HIV-1 reservoirs may limit the ability of these T-cells to identify and remove infected cells, which means that these cells can evade detection and continue to cause viral bounces.
In our study, we wanted to determine the frequency and pattern of T-cell escape mutations in HIV-1 reservoirs in people undergoing antiretroviral therapy," Warren said.
, the team measured HIV-1-specific T-cell response and isolated reservoir viruses in 25 people treated with HIV-specific T-cells.
Of these participants, four began antiviral treatment during acute HIV-1 infection, which meant that the level of the virus was early controlled, while the other 21 began antiviral treatment during chronic HIV-1 infection, which meant that a large number of viral mutations occurred before the level of the virus was controlled.
in each participant's HIV-1 proteomics, the team identified the T-cell table (the protein region that triggers the immune response).
they sequenced the HIV-1 "growth" virus from resting CD4-T cells and tested the effect of mutations in the T-cell's mesothet on the size of the T-cell response.
these strategies show that most (68%) of T-cells do not have any detectable escape mutations, meaning they can be identified by circulating T-cells.
"Our findings suggest that most HIV-specific T-cells in people receiving antiretroviral therapy can detect HIV virus with the ability to rebound after interruption of treatment," concluded Nilu Goonetilleke, a professor in the Department of Microbiology and Immunology.
suggests that T-cells may help control the virus's rebound and can be used in future treatment strategies for HIV.
Bioon.com Source: How immune cells can recognize-and-control-HIV when therapy isinterrupted Original Source: Joanna A Warren et al, The HIV-1 latent reservoir is largely resented to reeding T cells, eLife (2020). DOI: 10.7554/eLife.57246.