Eleven new genes affecting blood pressure discovered

New research from Queen Mary University of London has discovered 11 new DNA sequence variants in genes influencing high blood pressure and heart disease.

Identifying the new genes contributes to our growing understanding of the biology of blood pressure and, researchers believe, will eventually influence the development of new treatments. More immediately the study highlights opportunities to investigate the use of existing drugs for cardiovascular diseases.
The large international study, published today in the American Journal of Human Genetics, examined the DNA of 87,736 individuals to discover genetic variants associated with blood pressure traits. Validation of these sequence variants was performed in a further 68,368 individuals. This analysis led to the identification of 11 new genes.
Worldwide, raised blood pressure is estimated to cause 7.5 million deaths, about 12.8% of the total of all deaths. Genes and lifestyle factors (e.g., salt intake and obesity) are both known to be important risk factors.
Patricia Munroe, Professor of Molecular Medicine at Queen Mary University of London, comments: "Discovering these new genetic variants provides vital insight into how the body regulates blood pressure. With further research, we are hopeful it could lead to the development of new treatments for treating blood pressure and heart disease -- a leading cause of death worldwide."
Michael Barnes, Director of Bioinformatics, Barts and The London NIHR Cardiovascular Biomedical Research Unit, Queen Mary University of London, comments:
"By highlighting several existing drugs that target proteins which influence blood pressure regulation, our study creates a very real opportunity to fast-track new therapies for hypertension into the clinic."
 

Journal Reference:

1. Vinicius Tragante, Brendan J. Keating et al. Gene-centric Meta-analysis in 87,736 Individuals of European Ancestry Identifies Multiple Blood-Pressure-Related Loci. The American Journal of Human Genetics, 2014; DOI: 10.1016/j.ajhg.2013.12.016

Courtesy: ScienceDaily
 

Skin tumor vaccine shows promise in wild mice, rising hope for transplant patients

Papillomaviruses (linked to cervical cancer when they infect the mucosal tissue in the female reproductive tract) can also infect normal skin, where they cause warts and possibly non-melanoma skin cancer, mostly in immune-suppressed organ transplant patients. An article published on February 20th in PLOS Pathogens suggests that vaccination might prevent virus-associated benign and malignant skin tumors.

Transplant recipients need to take immunosuppressive drugs for the rest of their lives to prevent rejection of the transplanted organ. Among the side effects of these drugs, widespread abnormal skin growths have large impact on the patients' quality of life. These can also progress to skin cancer, for which transplant patients have a 250-fold elevated risk. Sabrina Vinzón and Frank Rösl, from the German Cancer Research Center in Heidelberg, and colleagues sought to test whether papillomavirus vaccination around the time of transplantation could prevent the skin lesions seen in patients.

They used a rodent species (the multimammate mouse) as a unique pre-clinical model in which skin papillomaviruses are present and usually transmitted to young offspring. This mimics the situation in humans--most of us are infected with skin papillomaviruses as children and carry the virus in skin cells for the rest of our lives. However, these animals are more sensitive to the virus than humans with an intact immune system: most of them spontaneously develop benign skin tumors as well as malignant ones.

The scientists made a vaccine against the rodent skin papillomavirus that was modeled on the highly efficient and widely approved HPV vaccine against human papillomaviruses that protects against cervical cancer and genital warts. When they tested that vaccine in their animals, they found that vaccination completely prevented the appearance of benign and malignant skin tumors.

Vaccination does not eliminate the virus, but virus numbers in skin cells are much lower in the vaccinated animals, so the vaccine succeeds in educating and boosting the immune system in a way that it can keep the virus in check. Importantly, it can do so even in mice treated with immune-suppressive drugs.

Given that the vaccine works even when given to already infected animals, and continues to suppress the virus even when they are treated with immune-suppressive drugs--conditions that are similar to immunosuppressed patients who were infected with papillomaviruses as children--the scientists conclude that "these findings provide the basis for the clinical development of potent vaccination strategies against cutaneous [skin] HPV infections and HPV-induced tumors, especially in patients awaiting organ transplantation."
 

Journal Reference:

1. Sabrina E. Vinzón, Ilona Braspenning-Wesch, Martin Müller, Edward K. Geissler, Ingo Nindl, Hermann-Josef Gröne, Kai Schäfer, Frank Rösl. Protective Vaccination against Papillomavirus-Induced Skin Tumors under Immunocompetent and Immunosuppressive Conditions: A Preclinical Study Using a Natural Outbred Animal Model. PLoS Pathogens, 2014; 10 (2): e1003924 DOI: 10.1371/journal.ppat.1003924 

Courtesy: ScienceDaily
 

If you think you have Alzheimer's, you just might be right, study suggests

A recent study suggests that self-reported memory complaints might predict clinical memory impairment later in life. Erin Abner, an assistant professor at the University of Kentucky's Sanders-Brown Center on Aging, asked 3,701 men aged 60 and higher a simple question: "Have you noticed any change in your memory since you last came in?"

That question led to some interesting results. "It seems that subjective memory complaint can be predictive of clinical memory impairment," Abner said. "Other epidemiologists have seen similar results, which is encouraging, since it means we might really be on to something."
The results are meaningful because it might help identify people who are at risk of developing Alzheimer's Disease sooner. "If the memory and thinking lapses people notice themselves could be early markers of risk for Alzheimer's disease, we might eventually be able to intervene earlier in the aging process to postpone and/or reduce the effects of cognitive memory impairment."
Abner, who is also a member of the faculty in the UK Department of Epidemiology, took pains to emphasize that her work shouldn't necessarily worry everyone who's ever forgotten where they left their keys.
"I don't want to alarm people," she said. "It's important to distinguish between normal memory lapses and significant memory problems, which usually change over time and affect multiple aspects of daily life."
 

Story Source:
The above story is based on materials provided by University of Kentucky. The original article was written by Laura Dawahare. Note: Materials may be edited for content and length.
 

Courtesy: ScienceDaily

 

Single chip device to provide real-time 3-D images from inside the heart, blood vessels

Researchers have developed the technology for a catheter-based device that would provide forward-looking, real-time, three-dimensional imaging from inside the heart, coronary arteries and peripheral blood vessels. With its volumetric imaging, the new device could better guide surgeons working in the heart, and potentially allow more of patients' clogged arteries to be cleared without major surgery.

The device integrates ultrasound transducers with processing electronics on a single 1.4 millimeter silicon chip. On-chip processing of signals allows data from more than a hundred elements on the device to be transmitted using just 13 tiny cables, permitting it to easily travel through circuitous blood vessels. The forward-looking images produced by the device would provide significantly more information than existing cross-sectional ultrasound.
Researchers have developed and tested a prototype able to provide image data at 60 frames per second, and plan next to conduct animal studies that could lead to commercialization of the device.
"Our device will allow doctors to see the whole volume that is in front of them within a blood vessel," said F. Levent Degertekin, a professor in the George W. Woodruff School of Mechanical Engineering at the Georgia Institute of Technology. "This will give cardiologists the equivalent of a flashlight so they can see blockages ahead of them in occluded arteries. It has the potential for reducing the amount of surgery that must be done to clear these vessels."
Details of the research were published online in the February 2014 issue of the journal IEEE Transactions on Ultrasonics, Ferroelectrics and Frequency Control. Research leading to the device development was supported by the National Institute of Biomedical Imaging and Bioengineering (NIBIB), part of the National Institutes of Health.
"If you're a doctor, you want to see what is going on inside the arteries and inside the heart, but most of the devices being used for this today provide only cross-sectional images," Degertekin explained. "If you have an artery that is totally blocked, for example, you need a system that tells you what's in front of you. You need to see the front, back and sidewalls altogether. That kind of information is basically not available at this time."
The single chip device combines capacitive micromachined ultrasonic transducer (CMUT) arrays with front-end CMOS electronics technology to provide three-dimensional intravascular ultrasound (IVUS) and intracardiac echography (ICE) images. The dual-ring array includes 56 ultrasound transmit elements and 48 receive elements. When assembled, the donut-shaped array is just 1.5 millimeters in diameter, with a 430-micron center hole to accommodate a guide wire.
Power-saving circuitry in the array shuts down sensors when they are not needed, allowing the device to operate with just 20 milliwatts of power, reducing the amount of heat generated inside the body. The ultrasound transducers operate at a frequency of 20 megahertz (MHz).
Imaging devices operating within blood vessels can provide higher resolution images than devices used from outside the body because they can operate at higher frequencies. But operating inside blood vessels requires devices that are small and flexible enough to travel through the circulatory system. They must also be able to operate in blood.
Doing that requires a large number of elements to transmit and receive the ultrasound information. Transmitting data from these elements to external processing equipment could require many cable connections, potentially limiting the device's ability to be threaded inside the body.
Degertekin and his collaborators addressed that challenge by miniaturizing the elements and carrying out some of the processing on the probe itself, allowing them to obtain what they believe are clinically-useful images with only 13 cables.
"You want the most compact and flexible catheter possible," Degertekin explained. "We could not do that without integrating the electronics and the imaging array on the same chip."
Based on their prototype, the researchers expect to conduct animal trials to demonstrate the device's potential applications. They ultimately expect to license the technology to an established medical diagnostic firm to conduct the clinical trials necessary to obtain FDA approval.
For the future, Degertekin hopes to develop a version of the device that could guide interventions in the heart under magnetic resonance imaging (MRI). Other plans include further reducing the size of the device to place it on a 400-micron diameter guide wire.
In addition to Degertekin, the research team included Jennifer Hasler, a professor in the Georgia Tech School of Electrical and Computer Engineering; Mustafa Karaman, a professor at Istanbul Technical University; Coskun Tekes, a postdoctoral fellow in the Woodruff School of Mechanical Engineering; Gokce Gurun and Jaime Zahorian, recent graduates of Georgia Tech's School of Electrical and Computer Engineering, and Georgia Tech Ph.D. students Toby Xu and Sarp Satir.
This research was supported by award number R01EB010070 from the National Institute of Biomedical Imaging and Bioengineering (NIBIB), part of the National Institutes of Health (NIH).
 

Journal Reference:

1. Gokce Gurun, Coskun Tekes, Jaime Zahorian, Toby Xu, Sarp Satir, Mustafa Karaman, Jennifer Hasler, F. Degertekin. Single-chip CMUT-on-CMOS front-end system for real-time volumetric IVUS and ICE imaging. IEEE Transactions on Ultrasonics, Ferroelectrics and Frequency Control, 2014; 61 (2): 239 DOI: 10.1109/TUFFC.2014.6722610

Courtesy: ScienceDaily
 

Study on flu evolution may change textbooks, history books

A new study reconstructing the evolutionary tree of flu viruses challenges conventional wisdom and solves some of the mysteries surrounding flu outbreaks of historical significance.

The study, published in the journal Nature, provides the most comprehensive analysis to date of the evolutionary relationships of influenza virus across different host species over time. In addition to dissecting how the virus evolves at different rates in different host species, the study challenges several tenets of conventional wisdom -- for example, the notion that the virus moves largely unidirectionally from wild birds to domestic birds rather than with spillover in the other direction. It also helps resolve the origin of the virus that caused the unprecedentedly severe influenza pandemic of 1918.
The new research is likely to change how scientists and health experts look at the history of influenza virus, how it has changed genetically over time and how it has jumped between different host species. The findings may have implications ranging from the assessment of health risks for populations to developing vaccines.
"We now have a really clear family tree of theses viruses in all those hosts -- including birds, humans, horses, pigs -- and once you have that, it changes the picture of how this virus evolved," said Michael Worobey, a professor of ecology and evolutionary biology at the University of Arizona, who co-led the study with Andrew Rambaut, a professor at the Institute of Evolutionary Biology at the University of Edinburgh. "The approach we developed works much better at resolving the true evolution and history than anything that has previously been used."
Worobey explained that "if you don't account for the fact that the virus evolves at a different rates in each host species, you can get nonsense -- nonsensical results about when and from where pandemic viruses emerged."
"Once you resolve the evolutionary trees for these viruses correctly, everything snaps into place and makes much more sense," Worobey said, adding that the study originated at his kitchen table.
"I had a bunch of those evolutionary trees printed out on paper in front of me and started measuring the lengths of the branches with my daughter's plastic ruler that happened to be on the table. Just like branches on a real tree, you can see that the branches on the evolutionary tree grow at different rates in humans versus horses versus birds. And I had a glimmer of an idea that this would be important for our public health inferences about where these viruses come from and how they evolve."
"My longtime collaborator Andrew Rambaut implemented in the computer what I had been doing with a plastic ruler. We developed software that allows the clock to tick at different rates in different host species. Once we had that, it produces these very clear and clean results."
The team analyzed a dataset with more than 80,000 gene sequences representing the global diversity of the influenza A virus and analyzed them with their newly developed approach. The influenza A virus is subdivided into 17 so-called HA subtypes -- H1 through H17 -- and 10 subtypes of NA, N1-N10. These mix and match, for example H1N1, H7N9, with the greatest diversity seen in birds.
Using the new family tree of the flu virus as a map showed which species moved to which host species and when. It revealed that for several of its 8 genomic segments avian influenza virus is not nearly as ancient as often assumed.
"What we're finding is that the avian virus has an extremely shallow history in most genes, not much older than the invention of the telephone," Worobey explained.
The research team, which included UA graduate student Guan-Zhu Han and Andrew Rambaut, a professor from the University of Edinburgh who is also affiliated with the U.S. National Institutes of Health, found a strong signature in the data suggesting that something revolutionary happened to avian influenza virus, with the majority of its genetic diversity being replaced by some new variant in a selective sweep in an extremely synchronous event.
Worobey said the timing is provocative because of the correlation of that sudden shift in the flu virus' evolution with historical events in the late nineteenth century.
"In the 1870s, an immense horse flu outbreak swept across North America," Worobey said, "City by city and town by town, horses got sick and perhaps five percent of them died. Half of Boston burned down during the outbreak, because there were no horses to pull the pump wagons. Out here in the West, the U.S. Cavalry was fighting the Apaches on foot because all the horses were sick. This happened at a time when horsepower was actual horse power. The horse flu outbreak pulled the rug out from under the economy."
According to Worobey, the newly generated evolutionary trees show a global replacement of the genes in the avian flu virus coinciding closely with the horse flu outbreak, which the analyses also reveal to be the closest relative to the avian virus.
"Interestingly, a previous research paper analyzing old newspaper records reported that in the days following the horse flu outbreak, there were repeated outbreaks described at the time as influenza killing chickens and other domestic birds," Worobey said. "That's another unexpected link in the history, and the there is a possibility that the two might be connected, given what we see in our trees."
He added that the evolutionary results didn't allow for a definitive determination of whether the virus jumped from horses to birds or vice versa, but a close relationship between the two virus species is clearly there.
With regard to humans, the research sheds light on a longstanding mystery. Ever since the influenza pandemic of 1918, it has not been possible to narrow down even to a hemisphere the geographic origins of any of the genes of the pandemic virus.
"Our study changes that," Worobey said. "It is now clear that most of its genome jumped from birds very close to 1918 in the Western Hemisphere, and there is a suggestion that it was North America in particular."
The results also challenge the accepted wisdom of wild birds as the major reservoir harboring the flu virus, from where it jumps to domestic birds and other species, including humans. Instead, the genetic diversity across the whole avian virus gene pool in domestic and wild birds often appears to trace back to earlier outbreaks of the virus in domestic birds, Worobey explained.
"People tend to think of wild birds as the source of everything, but we see a very strong indication of spillover from domestic birds to wild birds," he said. "It turns out the animals we keep for food and eggs may be substantially shaping the diversity of these viruses in the wild over time spans of decades. That is a surprise."
 

Journal Reference:

1. Michael Worobey, Guan-Zhu Han, Andrew Rambaut. A synchronized global sweep of the internal genes of modern avian influenza virus. Nature, 2014; DOI: 10.1038/nature13016

Courtesy: ScienceDaily
 

Cell cycle speed is key to making aging cells young again

 A fundamental axiom of biology used to be that cell fate is a one-way street -- once a cell commits to becoming muscle, skin, or blood it always remains muscle, skin, or blood cell. That belief was upended in the past decade when a Japanese scientist introduced four simple factors into skin cells and returned them to an embryonic-like state, capable of becoming almost any cell type in the body.

Researchers have identified a major obstacle to converting cells back to their youthful state -- the speed of the cell cycle, or the time required for a cell to divide.

Credit: Image courtesy of Yale University

 

Hopeful of revolutionary medical therapies using a patient's own cells, scientists rushed to capitalize on the discovery by 2012 Nobel Laureate Shinya Yamanaka. However, the process has remained slow and inefficient, and scientists have had a difficult time discovering a genetic explanation of why this should be.
In the Jan. 30 issue of the journal Cell, Yale School of Medicine researchers identified a major obstacle to converting cells back to their youthful state -- the speed of the cell cycle, or the time required for a cell to divide.
When the cell cycle accelerates to a certain speed, the barriers that keep a cell's fate on one path diminish. In such a state, cells are easily persuaded to change their identity and become pluripotent, or capable of becoming multiple cell types.
"One analogy may be that when temperature increases to sufficient degrees, even a very hard piece of steel can be malleable so that you can give it a new shape easily," said Shangqin Guo, assistant professor of cell biology at the Yale Stem Cell Center and lead author of the paper. "Once cells are cycling extremely fast, they do not seem to face the same barriers to becoming pluripotent."
Guo's team studied blood-forming cells, which when dividing undergo specific changes in their cell cycle to produce new blood cells. Blood-forming progenitor cells normally produce only new blood cells. However, the introduction of Yamanaka factors sometimes -- but not always -- help these blood-forming cells become other types of cells. The new report finds that after this treatment blood-forming cells tend to become pluripotent when the cell cycle is completed in eight hours or less, an unusual speed for adult cells. Cells that cycle more slowly remain blood cells.
"This discovery changes the way people think about how to change cell fate and reveals that a basic 'house-keeping' function of a cell, such as its cell cycle length, can actually have a major impact on switching the fate of a cell," said Haifan Lin, director of the Yale Stem Cell Center.
The study has other implications than explaining the bottleneck in reprogramming that makes it difficult to produce individualized pluripotent stem cells for research and therapy. Shangqin Guo noted that many human diseases are associated with abnormalities in establishing proper cell identity as well as abnormalities in cell cycle behavior.
Video: http://vimeo.com/59083655

 Journal Reference:

1. Shangqin Guo, Xiaoyuan Zi, Vincent P. Schulz, Jijun Cheng, Mei Zhong, Sebastian H.J. Koochaki, Cynthia M. Megyola, Xinghua Pan, Kartoosh Heydari, Sherman M. Weissman et al. Nonstochastic Reprogramming from a Privileged Somatic Cell State. Cell, 2014 DOI: 10.1016/j.cell.2014.01.020

Courtesy: ScienceDaily

 

 

Trick identified that aids viral infection

Scientists have identified a way some viruses protect themselves from the immune system's efforts to stop infections, a finding that may make new approaches to treating viral infections possible.

Scientists have discovered a defense system — built into some viruses — that may be vulnerable to treatment. The researchers studied alphaviruses similar to the Eastern equine encephalitis virus, pictured above in red. This virus is transmitted to humans and horses by mosquito bites.

Credit: Fred Murphy, Sylvia Whitfield/CDC

These include faking or stealing a molecular identification badge that prevents a cell from recognizing a virus.

Scientists at Washington University School of Medicine in St. Louis and elsewhere have found some viruses have another trick. They can block the immune system protein that checks for the identification badge.

The blocking structure is called a stem-loop, found at the beginning of the virus's genetic material. This is the first time scientists have found an immune-fighting mechanism built directly into the genetic material of a virus. They are looking for ways to disable it and searching for similar mechanisms that may be built into the genetic material of other disease-causing microorganisms.

"When the stem-loop is in place and stable, it blocks a host cell immune protein that otherwise would bind to the virus and stop the infectious process," said senior author Michael Diamond, MD, PhD, professor of medicine. "We found that changing a single letter of the virus's genetic code can disable the stem-loop's protective effects and allow the virus to be recognized by the host immune protein. We hope to find ways to weaken the stem-loop structure with drugs or other treatments, restoring the natural virus-fighting capabilities of the cell and stopping or slowing some viral infections."

Most life forms encode their genes in DNA. To use the instructions contained in DNA, though, cells have to translate them into a related genetic material, RNA, that can be read by a cell's protein-making machinery.

Some viruses encode their genes directly in RNA. Examples include West Nile virus and influenza virus, and the viruses that cause sudden acute respiratory syndrome (SARS), yellow fever and polio.

When a virus infects a cell, it co-opts the cell's protein-making machinery to make viral proteins. These proteins allow the virus to replicate. Copies of the virus break into other cells, repeat the process, and the infection spreads.

The researchers studied alphaviruses, a group of RNA viruses that cause fever, encephalitis and infectious arthritis. They showed that a single-letter change in the RNA of an alphavirus strengthened the stem-loop. When the structure was stable, a key immune system protein called Ifit1 was blocked from binding to the viral RNA and the infection continued unchecked. But when the stem-loop was unstable, Ifit1 would bind to the viral RNA and disable it, stopping the infectious process.

"Knowing about this built-in viral defense mechanism gives us a new opportunity to improve treatment of infection," Diamond said. "To control emergent infections, we must continue to look for ways that viruses have antagonized our natural defense mechanisms and discover how to disable them."

Story Source:
The above story is based on materials provided by Washington University in St. Louis. The original article was written by Michael C. Purdy. Note: Materials may be edited for content and length.
 

Courtesy: ScienceDaily

Detailed look at HIV in action: Researchers gain a better understanding of the virus through electron microscopy

The human intestinal tract, or gut, is best known for its role in digestion. But this collection of organs also plays a prominent role in the immune system. In fact, it is one of the first parts of the body that is attacked in the early stages of an HIV infection. Knowing how the virus infects cells and accumulates in this area is critical to developing new therapies for the over 33 million people worldwide living with HIV. Researchers at the California Institute of Technology (Caltech) are the first to have utilized high-resolution electron microscopy to look at HIV infection within the actual tissue of an infected organism, providing perhaps the most detailed characterization yet of HIV infection in the gut.

 

A tomographic reconstruction of the colon shows the location of large pools of HIV-1 virus particles (in blue) located in the spaces between adjacent cells. The purple objects within each sphere represent the conical cores that are one of the structural hallmarks of the HIV virus.

Credit: Mark Ladinsky/Caltech

The team's findings are described in the January 30 issue of PLOS Pathogens.
"Looking at a real infection within real tissue is a big advance," says Mark Ladinsky, an electron microscope scientist at Caltech and lead author of the paper. "With something like HIV, it's usually very difficult and dangerous to do because the virus is an infectious agent. We used an animal model implanted with human tissue so we can study the actual virus under, essentially, its normal circumstances."
Ladinsky worked with Pamela Bjorkman, Max Delbrück Professor of Biology at Caltech, to take three-dimensional images of normal cells along with HIV-infected tissues from the gut of a mouse model engineered to have a human immune system. The team used a technique called electron tomography, in which a tissue sample is embedded in plastic and placed under a high-powered microscope. Then the sample is tilted incrementally through a course of 120 degrees, and pictures are taken of it at one-degree intervals. All of the images are then very carefully aligned with one another and, through a process called back projection, turned into a 3-D reconstruction that allows different places within the volume to be viewed one pixel at a time.
"Most prior electron microscopy studies of HIV have focused on the virus itself or on infection of laboratory-grown cell cultures," says Bjorkman, who is also an investigator with the Howard Hughes Medical Institute. "Ours is the first major electron microscopy study to look at HIV interacting with other cells in the actual gut tissue of an infected animal model."
By procuring such detailed images, Ladinsky and Bjorkman were able to confirm several observations of HIV made in prior, in vitro studies, including the structure and behavior of the virus as it buds off of infected cells and moves into the surrounding tissue and structural details of HIV budding from cells within an infected tissue. The team also described several novel observations, including the existence of "pools" of HIV in between cells, evidence that HIV can infect new cells both by direct contact or by free viruses in the same tissue, and that pools of HIV can be found deep in the gut.
"The study suggests that an infected cell releases newly formed viruses in a semisynchronous wave pattern," explains Ladinsky. "It doesn't look like one virus buds off and then another in a random way. Rather, it appears that groups of virus bud off from a given cell within a certain time frame and then, a little while later, another group does the same, and then another, and so on."
The team came to this conclusion by identifying single infected cells using electron microscopy. Then they looked for HIV particles at different distances from the original cell and saw that the groups of particles were more mature as their distance from the infected cell increased.
"This finding showed that indeed these cells were producing waves of virus rather than individual ones, which was a neat observation," says Ladinsky.
In addition to producing waves of virus, infected cells are also thought to spread HIV through direct contact with their neighbors. Bjorkman and Ladinsky were able to visualize this phenomenon, known as a virological synapse, using electron microscopy.
"We were able to see one cell producing a viral bud that is contacting the cell next to it, suggesting that it's about to infect directly," Ladinsky says. "The space between those two cells represents the virological synapse."
Finally, the team found pools of HIV accumulating between cells where there was no indication of a virological synapse. This suggested that a virological synapse, which may be protected from some of the body's immune defenses, is not the only way in which HIV can infect new cells. The finding of HIV transfer via free pools of free virus offers hope that treatment with protein-based drugs, such as antibodies, could be an effective means of augmenting or replacing current treatment regimens that use small-molecule antiretroviral drugs.
"We saw these pools of virus in places where we had not initially expected to see them, down deep in the intestine," he explains. "Most of the immune cells in the gut are found higher up, so finding large amounts of the virus in the crypt regions was surprising."
The team will continue their efforts to look at HIV and related viruses under natural conditions using additional animal models, and potentially people.
"The end goal is to look at a native infection in human tissue to get a real picture of how it's working inside the body, and hopefully make a positive difference in fighting this epidemic," says Bjorkman.
 

Journal Reference:

1. Mark S. Ladinsky, Collin Kieffer, Gregory Olson, Maud Deruaz, Vladimir Vrbanac, Andrew M. Tager, Douglas S. Kwon, Pamela J. Bjorkman. Electron Tomography of HIV-1 Infection in Gut-Associated Lymphoid Tissue. PLoS Pathogens, 2014; 10 (1): e1003899 DOI: 10.1371/journal.ppat.1003899

 

 Courtesy: ScienceDaily