Researchers at Washington Medical University, USA, a paper in the journal Science
There was a time when people thought they had been sentenced to death after being infected with the AIDS (acquired immunodeficiency syndrome) virus (HIV).
AIDS is not so deadly.
In particular, with the advent of HAART therapy in which three or more anti-HIV agents are administered at once, the life expectancy of HIV-infected people has improved to a level similar to those of non-infected people.
However, there is a big difference between HIV positive and negative.
The infected person should first strictly follow antiretroviral therapy. This is because if you neglect it for a day, the latent HIV will reactivate.
Transmitting the virus to other people is also a serious problem.
Antiretroviral agents administered to AIDS block the replication and proliferation of viruses that have entered the body, but cannot prevent infection.
A treatment route has been revealed to reactivate the AIDS virus, which hibernates deep inside immune cells, and blocks infection at the source.
Human immune cells have an alarm system that detects the initial activation of certain HIV proteins.
On the 4th (local time), the research team of assistant professor Liang Shan of the University of Washington Medical School published a related paper in the journal Science.
HIV infects CD4+ T cells (helper T cells), causing immune deficiency.
For this infection to be established, the glycoprotein of HIV’gp 120′ must first bind to the CD4 molecule.
HIV-infected CD4-positive T cells eventually die due to excessive viral proliferation or attack by killer T cells.
Through this process, when the levels of CD4 and CD8 in the peripheral blood drop, cellular immunity is rapidly reduced.
Cell immunity refers to the killing of whole virus-infected cells by killer cells, and is differentiated from local immunity that attacks the virus before entering the blood or humoral immunity that attacks the virus invading the blood with antibodies.
In fact, it is almost impossible to eradicate hidden HIV in hibernation.
This is because HIV mutates very rapidly to avoid immune attacks.
HIV mutations are similar to spy disguises, who change their appearance in a flashy manner, and are insufficient for human immune systems to track.
The greatest achievement of this study is to discover an immune mechanism that breaks the disguise of HIV.
A more interesting point is the possibility of clearing out the inactive hiding virus of the infected person. If this treatment is successful, HIV-positive carriers can completely return to normal.
HIV requires the HIV protease (protein-degrading enzyme) to replicate and spread particles.
However, it was confirmed this time that human immune cells detect the activation of this enzyme.
It cannot detect viruses directly, but instead it is said to track the movement of the virus.
The research team also found an inflammation-modulating complex called CARD8 that acts like an alarm in immune cells.
CARD8 captured the activated HIV protease and induced apoptosis (programmed cell death) of infected cells.
The problem is that even if the HIV protease is not activated, HIV can survive long in cells.
In fact, the HIV protease does not function much inside the infected cell, but is activated when the virus leaves the infected cell.
The research team found that NNRTI (non-nucleic acid reverse transcriptase inhibitor) drugs, which have been used in the treatment of AIDS since the 1990s, induce early activation of HIV proteases.
However, NNRTI has this effect only when the virus wakes up from hibernation.
This means that NNRTIs cannot be used simultaneously because the virus hides in hibernation when anti-HIV drugs are administered.
The research team is reviewing a clinical trial in which hibernating HIV is first awakened and then NNRTI is administered.
Professor San said, “Through this study, we presented a guide for the development of drugs that eradicate hibernation HIV,” he said. “I would like to discover or develop a compound that works better than NNRTI even at low doses.”
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