Tag Archives: RNA

‘Good virus’ believed to help increase survival chances in Ebola and HIV infections

All viruses may not be harmful, says a study hinting at beneficial effect of some.

All viruses may not be harmful, says a study hinting at beneficial effect of some.

A common virus that infects billions at some point of their lives is believed to deliver some protection against other deadlier viruses like HIV and Ebola.

David O’Connor, a pathology professor at the University of Wisconsin in Madison, found the genetic fingerprints of the virus GBV-C in the records of 13 samples of blood plasma from Ebola patients.

While six of the 13 people who were co-infected with Ebola and GBV-C died, seven survived.

Combined with earlier studies that have hinted persistent infection with the virus slowed disease progression in some HIV patients, researchers think the virus could be beneficial.

The results could also simply mean that people aged 20 to 40 are more likely to be infected with GBV-C and more likely to survive Ebola.

“We’re very cautious about over-interpreting these results,” O’Connor told NPR. He is now waiting to get a bigger sample, to see if there really is a strong connection between GBV-C infection and survival.

The GB Virus-C came from a small monkey — a marmoset — that had been used in an experiment to diagnose a surgeon with hepatitis.

The virus infects a type of white blood cell and dampens part of the immune system. With HIV, the virus helps reduce inflammation, and that in turn helps slow the onset of Aids.

Cancer link

Similarly, it might also reduce inflammation in some people fighting off an Ebola infection.
However, the virus is not entirely harmless.

A National Institutes of Health study last year suggests a cancer link to the virus. People with a cancer of the lymphatic system, non-Hodgkin lymphoma, were seen to be more likely to be infected with GBV-C.

HIV mostly targets CD4 T lymphocytes, a cell involved in initiating an immune response. The virus hijacks the cell’s reproductive process to produce more copies of itself which infect and kill other cells.

Filoviruses like Ebola get all their genetic material from RNA, instead of DNA and most of the genetic information stored in the RNA codes for a handful of proteins as compared to about 20,000 in humans.

One of these proteins, glycoprotein, is suspected to play a big role in Ebola. A version of this protein is believed to bind to host cells, enter and replicate inside while another version is suspected to work by suppressing the immune system.

There is still much not known about the working of these two deadly viruses, which have also seen to mutate rapidly and deter drug treatments.

via IBM Times

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HIV can “cut & paste” parts in the human genome

genelights

For the first time, researchers have modified HIV virus particles so that they can simultaneously, as it were, ‘cut and paste’ in our genome via biological processes.

Developed by biologists from the Aarhus University, the technology makes it possible to repair genomes in a new way. It also offers new perspectives for treating several viral infections:

“Now we can simultaneously cut out the part of the genome that is broken in sick cells, and patch the gap that arises in the genetic information which we have removed from the genome. The new aspect here is that we can bring the scissors and the patch together in the HIV particles in a fashion that no one else has done before,” says associate professor in genetics Jacob Giehm Mikkelsen from Aarhus University.

HIV has been known for being able to alter the human genome – as a matter of fact, this is the mechanism for every retrovirus out there – that’s just how they work. This mechanism is extremely interesting, and at a very basic level, it works like this: when a retrovirus enters a cell, its genetic information is in the form of RNA, which is different to DNA. The retrovirus uses a special enzyme to make a DNA copy of the RNA genome of the virus; this DNA copy travels to the nucleus of the cell, where it is spliced into the host’s genome, thus ordering it to create new virus particles.

What this research team has done is develop a technique that increases the safety of the cutting process, the so-called “gene editing”:

“In the past, the gene for the scissors has been transferred to the cells, which is dangerous because the cell keeps on producing scissors which can start cutting uncontrollably. But because we make the scissors in the form of a protein, they only cut for a few hours, after which they are broken down. And we ensure that the virus particle also brings along a small piece of genetic material to patch the hole,” says Jacob Giehm Mikkelsen.

According to them, there is no risk of further infection, and it has no negative effects:

“We call this a ‘hit-and-run’ technique because the process is fast and leaves no traces”.

This kind of treatment is called gene therapy – it has been proposed for quite a while, but so far, it has only been trialled with limited success – working around a person’s DNA is extremely dangerous, and cancer is always a potential result. However, if their results are as good as they claim, this might finally overcome that hurdle.

HIV infection is one of the areas where the researchers want to make use of the technique, and here the goal is to stop a specific gene from functioning – something that the protein scissors used here can do.

“By altering relevant cells in the immune system (T cells) we can make them resistant to HIV infection and perhaps even at the same time also equip them with genes that help fight HIV.

“So in this way HIV can in time become a tool in the fight against HIV,” says postdoc and PhD Yujia Cai of the research team.

The scientific paper is available here: Targeted genome editing by lentiviral protein transduction of zinc-finger and TAL-effector nucleases

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A Cure for HIV/AIDS Has Got a Step Closer!

Listen to this article instead [audio http://www.lass.org.uk/files/uploads/120802.mp3]

HIV is an exceptional adversary. It is more diverse than any other virus, and it attacks the very immune cells that are meant to destroy it. If that wasn’t bad enough, it also has a stealth mode. The virus can smuggle its genes into those of long-lived white blood cells, and lie dormant for years. This “latent” form doesn’t cause disease, but it’s also invisible to the immune system and to anti-HIV drugs.

When the virus awakens, it can trigger new bouts of infection – a risk that forces HIV patients to stay on treatments for life. It’s clear that if we’re going to cure HIV for good, we need some way of rousing these dormant viruses from their rest and eliminating them.

Now, a cure for HIV/AIDS has got a step closer after scientists found that a common cancer drug can purge the disease as it lies dormant in the body.  Current treatments are effective at reducing levels of the disease in the bloodstream – but a drug that can ‘knock out’ the disease when it lies dormant is thought to be key to a cure.

A team of US scientists led by David Margolis has found that vorinostat – a drug used to treat lymphoma – can do exactly that. It shocks HIV out of hiding. While other chemicals have disrupted dormant HIV within cells in a dish, this is the first time that any substance has done the same thing in actual people.

At this stage, Margolis’s study just proves the concept – it shows that disrupting HIV’s dormancy is possible, but not what happens afterwards. The idea is that the awakened viruses would either kill the cell, or alert the immune system to do the job. Drugs could then stop the fresh viruses from infecting healthy cells. If all the hidden viruses could be activated, it should be possible to completely drain the reservoir. For now, that’s still a very big if, but Margolis’s study is a step in the right direction.

HIV enters its dormant state by convincing our cells to hide its genes. It recruits an enzyme called histone deacetylase (HDAC), which ensures that its genes are tightly wrapped and cannot be activated. Vorinostat, however, is an HDAC inhibitor – it stops the enzyme from doing its job, and opens up the genes that it hides.

It had already proven its worth against HIV in the lab. Back in 2009, three groups of scientists(including Margolis’ team) showed that vorinostat could shock HIV out of cultured cells, producing detectable levels of viruses when they weren’t any before.

To see if the drug could do the same for patients, the team extracted white blood cells from 16 people with HIV, purified the “resting CD4 T-cells” that the virus hides in, and exposed them to vorinostat. Eleven of the patients showed higher levels of HIV RNA (the DNA-like molecule that encodes HIV’s genes) – a sign that the virus had woken up.

Eight of these patients agreed to take part in the next phase. Margolis gave them a low 200 milligram dose of vorinostat to check that they could tolerate it, followed by a higher 400 milligram dose a few weeks later. Within just six hours, he found that the level of viral RNA in their T-cells had gone up by almost 5 times.

These results are enough to raise a smile, if not an outright cheer. We still don’t know how extensively vorinostat can smoke HIV out of hiding, or what happens to the infected cells once this happens. At the doses used in the study, the amount of RNA might have gone up, but the number of actual viral particles in the patients’ blood did not. It’s unlikely that the drug made much of a dent on the reservoir of hidden viruses, so what dose should we use, and over what time?

Vorinostat’s actions were also very varied. It did nothing for 5 of the original 16 patients. For the 8 who actually got the drug, some produced 10 times as much viral RNA, while others had just 1.5 times more. And as you might expect, vorinostat comes with a host of side effects, and there are concerns that it could damage DNA. This study could be a jumping point for creating safer versions of the drug that are specifically designed to awaken latent HIV, but even then, you would still be trying to use potentially toxic drugs to cure a long-term disease that isn’t currently showing its face. The ethics of doing that aren’t clear.

Steven Deeks, a HIV researcher from the University of California San Francisco, talks about these problems and more in an editorial that accompanies the new paper. But he also says that the importance of the study “cannot be over­stated, as it provides a rationale for an entirely new approach to the management of HIV infection”.

Progress is being made every day, don’t believe us? – Check out the related articles below!

Original Articles via Discover Magazine and Mail Online

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