Protein that destroys HIV discovered
August 23, 2010
Loyola University researchers have identified the key components of a protein called TRIM5a that destroys HIV in rhesus monkeys.
The finding could lead to new TRIM5a-based treatments that would knock out HIV in humans, said senior researcher Edward M. Campbell, PhD, of Loyola University Health System.
Campbell and colleagues report their findings in an article featured on the cover of the Sept. 15, 2010 issue of the journal Virology, now available online.
In 2004, other researchers reported that TRIM5a protects rhesus monkeys from HIV. The TRIM5a protein first latches on to a HIV virus, then other TRIM5a proteins gang up and destroy the virus.
Humans also have TRIM5a, but while the human version of TRIM5a protects against some viruses, it does not protect against HIV.
Researchers hope to turn TRIM5a into an effective therapeutic agent. But first they need to identify the components in TRIM5a that enable the protein to destroy viruses. “Scientists have been trying to develop antiviral therapies for only about 75 years,” Campbell said. “Evolution has been playing this game for millions of years, and it has identified a point of intervention that we still know very little about.”
TRIM5a consists of nearly 500 amino acid subunits. Loyola researchers have identified six 6 individual amino acids, located in a previously little-studied region of the TRIM5a protein, that are critical in the ability of the protein to inhibit viral infection. When these amino acids were altered in human cells, TRIM5a lost its ability to block HIV-1 infection. (The research was done on cell cultures; no rhesus monkeys were used in the study.)
By continuing to narrow their search, researchers hope to identify an amino acid, or combination of amino acids, that enable TRIM5a to destroy HIV. Once these critical amino acids are identified, it might be possible to genetically engineer TRIM5a to make it more effective in humans. Moreover, a better understanding of the underlying mechanism of action might enable the development of drugs that mimic TRIM5a action, Campbell said.
In their research, scientists used Loyola’s wide-field “deconvolution” microscope to observe how the amino acids they identified altered the behavior of TRIM5a. They attached fluorescent proteins to TRIM5a to, in effect, make it glow. In current studies, researchers are fluorescently labeling individual HIV viruses and measuring the microscopic interactions between HIV and TRIM5a.
More info: Loyola University Health System news

Comments (5)
by Richard Badge
An interesting paper, but I have to agree with throwaway is taken – site directed mutagenesis can tell you that a particular motif when disrupted can alter a proteins activity, but this could be true of many sites… I am much more excited by the work on Trim5a – cyclophilin fusion genes (Neagu et al 2009 PMID: 19741300 and Dietrich et al 2010 PMID: 20554781).
by astronghope24
Alright so this is going to sound kind of crazy right now but today I had a very intense day with nature and it was just a weird day all together but i read this earlier and think it is a great step in finding a cure for HIV! upon pondering this most of my day I came upon a daddy long leg spider and then it occurred to could spider zenom help identify or modify the amino acids of the cell. I learned that certain venoms the potential medical uses of spider venoms are largely due to their selectivity and affinity for ion channels [proteins that allow ions to cross cell membranes] and other receptors. This makes them suitable for studying cell function and for designing therapeutic drugs. Just a thought I was really pondering today. Im probably way off though! good luck! and keep up the great research!
by RobinSongs
“but bad in that they will probably lead to risky behavior re-emerging in sexual activities”.
Virtual Reality will take care of that.
by throwawayistaken
Former assistant to postdoc in top-5 HIV lab here, throwaway acct. We’ve known and been doing research about Trim5 for years and years. This research isn’t very helpful — it deserves no more attention than other steps in current research.
Background: All primates have this protein. Trim5 in humans is usually hopeless against HIV but strong against SIV (Simian IV, the prevalent sister disease among species of primates. Yes, that means your immune to an ape STD — don’t test it, you aren’t immune to some others). In rhesus/spider monkeys, Trim5 has serious potency, rendering some breeds totally immune to all strains of SIV & HIV. And we’ve known for 5+ years which chains of the Trim5 protein are different across species, narrowing down the important areas.
Read carefully what they have advanced:
When these amino acids were altered in human cells, TRIM5a lost its ability to block HIV-1 infection.
They’ve discovered that they could make Trim5a ineffective against HIV-1 by altering a few amino acids. The step forward is that this is more specific than previous work in altering the protein — before, we had it narrowed down to short chains, not individual amino acids.
However, we’ve been disabling Trim5 by removing larger, less precise sections for years. More importantly, disabling a protein is not the same as finding it’s effective areas, or “active zones”. I can disable almost any amino acid critical to a protein’s folding and change it’s shape to render it ineffective, but that doesn’t tell me anything about its “active zones”. It’s like disabling a car by breaking its axle — the car doesn’t go, but I can’t conclude that I’ve located the car’s engine.
source: http://www.reddit.com/r/science/comments/d4lhp/protein_that_destroys_hiv_discovered/
by JohnVKaravitis
John V. Karavitis CONGRATULATIONS! This discovery is a milestone in the fight against AIDS! GOOD JOB! And think about it, this discovery could also pave the way for a complete cure for other viral diseases such as Herpes. Now, the thing to remember is that public education efforts must still be made to ensure that no other virus gains a foothold and spreads like AIDS. Viruses mutate all the time, and the successor to AIDS may not be subject to this particular method of attack. So, discoveries like this are good, but bad in that they will probably lead to risky behavior re-emerging in sexual activities. P.S. I found out about this article through Twitter. Twitter rocks! John V. Karavitis