Many young people are dying due to aids in this world but
why the scientists didn't invent vaccine? decades, a successful HIV vaccine has
been the Holy Grail for researchers around the globe. Yet despite years of
research and millions of dollars of investment, that goal has still yet to be
achieved. Recent research by Oregon Health & Science University scientists
explains a decades-old mystery as to why slightly weakened versions of the
monkey AIDS virus were able to prevent subsequent infection with the fully
virulent strain, but were too risky for human use, and why severely compromised
or completely inactivated versions of the virus were not effective at all.
The research was conducted at OHSU's Vaccine and Gene
Therapy Institute and is published online in the journal Nature Medicine.
Traditionally, there have been two methods for creating
vaccines to combat infectious disease. The first approach utilizes a live, yet
weakened strain of the disease in question. This weakened strain is not strong
enough to cause illness yet potent enough to activate the immune system so that
it can detect and fight a disease if it enters the body in the future. The
second approach makes use of a dead form of the disease. As with the other
approach, the introduction of the disease in a safe form educates and prepares
the body for a possible future invasion.
In the early 1990s, a slightly weakened version of SIV,
the monkey counterpart to HIV, was shown to protect monkeys for infection with
the fully virulent version, but this weakened version was still able to cause
AIDS in some monkeys and the protection was lost if the vaccine virus was
further weakened.
"Efforts to develop a live attenuated virus are
analogous to the tale of 'Goldilocks and the Three Bears,'" explained
Louis Picker, M.D., associate director of the OHSU Vaccine and Gene Therapy
Institute. "The field was looking for a vaccine that was 'not too hot,' or
'not too cold,' but 'just right.' The problem was that it appears that
weakening a virus to the level that is 'just right' is impossible. However, we
thought that understanding the mechanism responsible for the protection
afforded by the too-dangerous-for clinical-use attenuated vaccine would allow
us to design a vaccine that would be both effective and safe."
The newly published research shows that the protection is
due to anti-viral T cells maintained in lymphoid tissue by persistent live
attenuated virus; weakening the virus prevents this persistence and curtails
protection. Thus, unlike most vaccines, an effective HIV vaccine might have to
persist in the body to be effective.
Picker's group has developed another persistent virus
named cytomegalovirus (CMV) engineered to express SIV or HIV proteins and serve
as the transport system (vector) used to raise protective immune responses
against these AIDS-causing viruses. In May 2011, the Picker lab published
findings that demonstrated how immune responses elicited by their vaccine
candidate were able to completely control SIV in a significant number of
exposed animals.
CMV is a persistent virus that most people carry, causes
few or no symptoms, and elicits very strong cellular responses that are
maintained for life. These immune responses are characterized by a type of T
cell called an effector memory T cell that has potent anti-viral function and
localizes in the same tissues targeted by the AIDS-causing viruses. Picker and
his team hypothesize that CMV vector-generated anti-HIV responses would be
constantly on the alert for HIV and would be able to intercept and stop HIV
infection immediately after exposure.
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