Michigan research likely to make HIV treatment more effective
It can easily be spelt as the good news for all the HIV patients worldwide. University of Michigan scientists have provided the most detailed picture yet of a key HIV accessory protein that foils the body’s normal immune response. Based on the research, the team is searching for new drugs that may someday allow infected people to be cured and no longer need today’s AIDS drugs for a lifetime.
In people infected with HIV (human immunodeficiency virus), the virus that causes AIDS, there’s an unsolved problem with current anti-viral drugs. Though life-saving, they cannot root the virus out of the body. Infected cells are able to live on, undetected by the immune system, and provide the machinery for the virus to reproduce and spread.
The team of the researchers show how Nef disables two key immune system players inside an infected cell. These are molecules called major histocompatability complex 1 proteins (MHC-1) that present HIV antigens to the immune system, and CD4, the cell-surface receptor that normally locks onto a virus and allows it to enter the cell.Collins likens MHC-1 to motion detectors on a house, which send the first signal to a monitoring station if an invader breaks in.
By in effect pushing the MHC-I proteins into an infected cell’s “trash bin” so they fail to alert the T lymphocytes, Nef’s actions allow active virus to hide undetected and reproduce. Also, once a cell has been infected, Nef destroys CD4. The result is that this encourages new virus to spread to uninfected cells.In developing countries, the new drugs could have a huge impact. Today, children born with HIV infection start taking the existing anti-HIV drugs at birth.
It’s very hard to continue costly treatments for a lifetime. But if children could be cured within a few years, global HIV treatment efforts could spread their dollars further and be much more successful, she says.Nef’s activities are variable and complex. But the research team’s findings suggest that the many pathways involved may end in a final common step. That could make it possible to find a drug that could block several Nef functions.
Source: EurekAlert
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