A research team led by Dr. John Young, professor at the Salk Institute for Biological Studies, and Dr. Sumit Chanda, associate professor at Sanford-Burnham, was awarded a $21 million Program Project Grant from the National Institutes of Health (NIH). This funding will allow the team to analyze the innate immune response (the body’s earliest defenses) against HIV infection using a systems biology approach. This large-scale initiative aims to increase our understanding of all the body’s cellular and molecular factors that work together to respond to HIV-1 infection and how these factors influence a patient’s prognosis.The project will bring together a multidisciplinary team of 13 research groups at seven institutions to uncover the cellular machinery that represents the first line of defense against HIV, the cause of AIDS.
“The events that occur immediately after exposure to HIV, which determines the ability of the virus to establish infection and ultimately shape the course of the disease, are very poorly understood,” said Dr. Chanda. “This grant funds a multi-center consortium that will integrate cutting edge technologies in systems biology and next-generation sequencing with world-leading expertise in immunology and virology to decode and model the early molecular events that occur after HIV enters the body. These projects will be fundamental towards the development of safe and effective HIV vaccines, as well as novel preventative therapies for HIV.”
Read more about the project in a recent San Diego Union-Tribune article.
is it true that hiv is can not contant with intrucment like,razu bleda like babing salon and oder equiment that can cuase hiv .?
1. As known to me that HIV viruses attack only helper T-cells, ultimately causing their death.
What about the receptors present on the helper T-cells? Are they specific only to HIV viruses or the various other antigens.?
2. Why isn’t HIV transmitted through mosquitoes as vector?
3. Why isn’t HIV transmitted through mosquitoes as vector?
Hello. This is an idea or project intended to specificaly kill HIV-Infected cells.
This project is an expression of a willing desire, not a strictly and scientifically elaborated one. Knowing this limitation I hope there is a clear concept behind the way is written.
HIV Gene Therapy – A Chimerical DNA Vector to Specifically Kill HIV-Infected Cells
Introduction
During antiretroviral therapy HIV virions remain undetectable in serum. Nonetheless, after a long period of successful antiretroviral therapy, the integrated DNA (provirus) persists in reservoirs and reactivates when HAART is suspended. Besides, there is a minimum level of replication that preserves those reservoirs.
General objective
To create a vector able to specifically eradicate HIV-infected cells.
Specific objectives
To proceed with a three phases project consisting in evaluation of chimerical DNA integration in infected cells, its expression in animals, and its potential efficiency for specific killing of HIV-infected cells.
The idea
To eliminate selectively HIV-infected cells, it could be created a vector able to enter any cell but capable only to interact with those cells carrying the virus within them. That would be possible if the vector had a DNA resistant to cell degradation that bears a gene codifying for protein that triggers apoptosis. In this way, the project is to build up a DNA similar to HIV cDNA (Preintegration Complex – PIC) substituting the pol region with caspase-3. So, when the vector reaches the cytoplasm it will release de DNA that will bind to viral and human proteins (that are regularly bound to PIC) and it will migrate to the nucleus, and eventually be integrated. In a non-infected cell it will be finally degraded. It is known that PIC is quite resistant to cell degradation due to its particular composition and shape that let it associate with viral and cellular proteins. Furthermore, the vector envelope should not trigger an immune response because this therapy is intended to last for a period (re-inoculation), concomitantly with HAART.
The chimerical DNA vector cuold be a DNA with an insertion of caspase-3 gene replacing the pol segment, within a lipidic envelope: liposome.
Dr. Dowdy et al. (1999) demonstrated that a fusion protein (Tat-Caspase 3) was only active in presence of viral components (Pro) and innocuous in non-infected cells. The difference between a fusion protein and a chimerical DNA integrated as a provirus is the degree of Caspase 3 (resulting from chimerical DNA expression) available in the cytoplasm. So every time there is a transcription activation of HIV provirus, should be equally induced chimerical-DNA transcription, leading to mRNA translation, in which be included Caspase 3. In a replicative scenario there would also be segregation of mixed or pure non-infective virions containing chimerical RNA (lacking pol).
Project
To test this hypothesis the project could be divided in three phases.
In phases designed for animals the groups should include infected and non-infected animals with and without antiretroviral therapy.
Phase 1
Create the chimerical DNA vector consisting in the above mentioned HIV sequence but replacing pol with a reporter gene (i.e.: GFP coding gene) instead of caspase 3.
Inoculate on lymphocyte cultures (infected and non-infected) and evaluate.
Depending on results we could proceed to the next phase.
Phase 2
Inoculate the same vector of phase 1 in mice sensitive to HIV infection. As planned before, infected and non-infected mice. If the reporter is the GFP, we could evaluate fluorescence in tissues and blood.
Depending on results we could proceed to the next phase.
Phase 3
Replace the reporter gene with Caspase 3 gene and re-test in mice, looking for recovery (provirus load).
Final note: I am trying to participate in questions and answers in a colaborative and anonymous way , trusting in your good will. It is easy finding an IP address. I beg you do not focus on that
What Happens when HIV in Environmental temperature..?
Does silver nano or colloidal silver have the ability to suppress and sometimes destroy the hiv virus?
Why isn’t HIV transmitted through mosquitoes as vector?
Thanks for your question, Subrata! Here’s a great response from scientists at Rutgers University: http://www.rci.rutgers.edu/~insects/aids.htm. In short, HIV can’t survive in a mosquito’s gut long enough to be transmitted to another person.
Cheers,
Heather
As known to me that HIV viruses attack only helper T-cells, ultimately causing their death.
What about the receptors present on the helper T-cells? Are they specific only to HIV viruses or the various other antigens?
If they are specific to antigens then they must not respond to HIV viruses or the receptors on the HIV virus.
DO HIV virus can be kill by uv rays ?if yes then at what point?