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Monkeys vaccinated against SIV survive longer after infection

Results of two new studies sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), a component of the National Institutes of Health (NIH), suggest that even if an HIV vaccine offers imperfect protection against the virus, it might provide vaccinated individuals with an important benefit: a significant survival advantage after infection. “The worldwide need for an HIV vaccine is profound,” says Elias A. Zerhouni, M.D., director of the NIH. “In 2005, more than 11,000 people became infected with HIV every day. If that rate continues unchecked, the virus is going to infect another 40 million people during the coming decade.” “Although our ultimate goal is to have a vaccine that completely blocks HIV infection, this research suggests a potential benefit of even a partially effective vaccine,” says NIAID Director Anthony S. Fauci, M.D.

Published in this week’s issue of Science and this month’s issue of the Journal of Experimental Medicine, the studies also identified a measurable marker of SIV vaccine effectiveness in monkeys — something known as an immune correlate of vaccine efficacy. Further study is needed to determine if the immune correlate could predict the effectiveness of a vaccine against HIV in humans. “Having an immune correlate of vaccine efficacy could markedly reduce the time it takes to evaluate whether a candidate HIV vaccine works in people,” says VRC Director Gary J. Nabel, M.D., Ph.D. “The significance of this discovery is clearly worth evaluating in humans and may considerably accelerate future efficacy trials.”

The SIV vaccine regimen used in the two studies was a simplified version of a preventive human HIV vaccine strategy developed by VRC scientists and currently undergoing Phase II human clinical trials in the United States, the Caribbean and sub-Saharan Africa. Current plans call for testing the efficacy of the vaccine in large-scale human clinical trials some time next year. To examine the theory that some imperfect HIV vaccines may still allow infected people to live longer and healthier lives, Drs. Letvin and Roederer and their colleagues sought to determine if SIV vaccines confer such a survival advantage to monkeys.

They found that the best way to predict survival after a vaccinated monkey is infected with SIV is by measuring, early in infection, levels of a specific subset of immune cells known as the memory CD4+ T cells. Memory CD4+ T cells are T cells that have been activated by bacteria and viruses upon first exposure and are primed to act more quickly upon reinfection. Of the approximately one trillion T cells in the average adult, more than half are memory cells. Normally, a rapid and significant loss of these memory CD4+ T cells occurs early on in SIV infection: about ten days into the infection, when the levels of virus in the bloodstream are at their peak, up to 80 percent of the memory CD4+ T cells in some tissues became infected, and ultimately, nearly all of those memory CD4+ T cells are lost.

But vaccinating the monkeys can lessen this damage to the immune system, Dr. Roederer and his colleagues found. In their study of six vaccinated monkeys and six unvaccinated monkeys exposed to SIV, the vaccinated group had about 3 to 5 times fewer memory CD4+ T cells infected and destroyed. “If the virus wipes out only a fraction of the memory CD4+ T cells that it might otherwise destroy, that should allow [the animals] to live longer,” Dr. Roederer says. Likewise, he adds, if HIV vaccines can prevent the destruction of these memory cells in humans, it may be possible to provide people with longer, healthier lives.

In Dr. Letvin’s study, he and his colleagues looked at the effect of preserving the memory CD4+ T cells over the long term. A total of 30 monkeys — 24 vaccinated and six unvaccinated controls — were infected with SIV and followed for nearly three years. The vaccine helped control the infection for the first 112 days, but thereafter, the virus levels and total CD4+ counts in the vaccinated and unvaccinated animals did not differ significantly. But the vaccine protected the memory CD4+ T cells from the virus early on, and the levels of memory CD4+ T cells remained at significantly higher levels in the vaccinated animals for the 850 days they were studied. “This [early protection] had huge consequences for the development of disease,” says Dr. Letvin. “When infection did occur, the monkeys preserved their memory CD4+ T cells better and lived longer.”

Moreover, the researchers found that measuring a subset of the memory CD4+ T cells, so-called central memory CD4+ T cells, could help predict how the monkey would fare in the long run. Since these new studies indicate that the central memory CD4+ T cell counts appear to be a crucial predictor of long-term health, blood samples from human clinical trial participants might now be examined for this marker. That way, says Dr. Letvin, scientists can gauge how well a vaccine will perform simply by measuring the central memory cell levels in the first few months after infection.

Science Daily
July 3, 2006

Original web page at Science Daily

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Temple monkeys and health implications of commensalism, Kathmandu, Nepal

The threat of zoonotic transmission of infectious agents at monkey temples highlights the necessity of investigating the prevalence of enzootic infectious agents in these primate populations. Biological samples were collected from 39 rhesus macaques at the Swoyambhu Temple and tested by enzyme-linked immunosorbent assay, Western blot, polymerase chain reaction, or combination of these tests for evidence of infection with rhesus cytomegalovirus (RhCMV), Cercopithecine herpesvirus 1 (CHV-1), simian virus 40 (SV40), simian retrovirus (SRV), simian T-cell lymphotropic virus (STLV), simian immunodeficiency virus (SIV), and simian foamy virus (SFV). Antibody seroprevalence was 94.9% to RhCMV (37/39), 89.7% to SV40 (35/39), 64.1% to CHV-1 (25/39), and 97.4% to SFV (38/39). Humans who come into contact with macaques at Swoyambhu risk exposure to enzootic primateborne viruses. We discuss implications for public health and primate management strategies that would reduce contact between humans and primates.

Most pathogens that affect humans are thought to have originated in animals and subsequently evolved to successfully parasitize human populations. Proximity and physical contact between animals and humans provide the opportunity for infectious agents to pass between the groups. Whether a particular infectious agent can successfully make the cross-species jump depends in part on the new host environment. By virtue of their genetic, physiologic, and behavioral similarity to humans, nonhuman primates (hereafter referred to as primates) are particularly likely sources of emerging infectious agents with the capacity to infect humans, and primate-to-human cross-species transmission of infectious agents has become a focus of scientific inquiry. Because human-primate contact is common in Asia, this continent is a rich area in which to pursue this research. We examine the prevalence of selected enzootic primateborne viruses in a population of rhesus macaques (Macaca mulatta) that lives in close proximity to humans.

Monkey temples can be found throughout South and Southeast Asia, where primates play a role in Hindu and Buddhist culture. Macaque species, because they can thrive in human-altered environments, are the primates most often associated with temples. Extensive, unregulated, and often close contact between humans and primates occurs at these sites. Persons who live or work in or around monkey temples are among those who frequently come into contact with temple monkeys. Other persons may come into contact with temple macaques when they visit for purposes of worship, recreation, or tourism. Worldwide, monkey temples may account for more human-primate contact than any other context.

Swoyambhu Temple is 1 of 2 temple sites in the densely populated Kathmandu valley with a large population of free-ranging rhesus monkeys. As 1 of the region’s oldest and most important Buddhist holy places, Swoyambhu has been designated a world heritage site and continues to play a vibrant role in Kathmandu’s cultural life. In addition to the Tibetan monks, Brahmin priests, and Newar nuns who live on the site, a brisk flow of local worshipers and visitors from around the world passes through Swoyambhu. Persons who live and work in and around Swoyambhu share common water sources with the macaques and report that the macaques frequently invade their homes and gardens in search of food. The macaques at Swoyambhu have become a tourist attraction in their own right, and many visitors interact with the monkeys, often by feeding or teasing them. A growing literature documents human-macaque interactions at monkey temples in Asia. Macaques climb on the heads and shoulders of visitors, which may bring macaque body fluids into contact with visitors’ eyes and nasal and oral mucosa, potential portals of entry for infectious agents. Visitors may also be bitten or scratched by macaques during aggressive encounters, resulting in transcutaneous exposure to infectious agents present in macaque body fluids.

Emerging Infectious Diseases
June 20, 2006

Original web page at Emerging Infectious Diseases

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Testing on apes ‘might be needed’

Ministers should not rule out the possibility of allowing apes to be used in experiments, the head of the UK’s Medical Research Council (MRC) has said. In 1997, the government said it would never approve ape research because they were too similar to humans, but there is no law prohibiting the practice. Professor Colin Blakemore said such research was “essential” if it was the only way to cure a particular disease. Professor Blakemore’s comments came as campaigners for and against animal testing staged two separate protests in the row over Oxford University’s new £20m animal research laboratory. Supporters of animal testing were holding a rally in Oxford, while anti-vivisection campaigners were demonstrating in Moreton-in-Marsh, Gloucestershire.

Currently 2,800 non-human primates are used in medical research, but the Royal Society and the Academy of Medical Sciences are assessing whether genetically modified rats and mice could be used instead. A group of leading scientists has defended the use of primates in a booklet – Primates in Medical Research – which was published jointly by the MRC and the Wellcome Trust. Professor Blakemore told BBC Radio 4’s Today programme it was “not surprising” that many people were against research, as they were constantly told it was “unbelievably cruel” and “achieved nothing”. He added: “What we have seen in the last few years, against a background of ridiculous extremism, is more willingness to discuss openly when and where some animal research is necessary.

“The public have listened. They don’t like the idea. Who does? But they have realised that it is essential.” He said the final test for any drug or treatment had to be on humans, but added that 60% of potential drugs were rejected at the animal testing stage. These experiments are investigating diseases and conditions such as Parkinson’s, obsessive compulsive disorder, schizophrenia, HIV and strokes. However, the British Union for the Abolition of Vivisection (Buav) is publishing a report, due out on Monday, which calls for a ban on testing on any non-human primates. The publication has been backed by the world famous primatologist Jane Goodall, who described the testing as “unethical”.
Professor Colin Blakemore said: “In reality, most people do not know – and do not want to know – the grim reality of what happens to non-human primates in laboratories. “Not only are many experiments on them unethical, many are unnecessary; and their results may be misleading because they were developed at a time when scientists knew little about the effect of stress on the immune system.” Professor Sandy Thomas, director of the Nuffield Council on Bioethics, said: “It is important to be aware that research involving the great apes, such as gorillas, chimpanzees and orangutans, is not prohibited directly by law. “However, licences for this type of research are not granted as a matter of current Home Office policy. “The emergence of new diseases may mean that a reassessment of this policy is required in the future. On the other hand, the continued development of non-animal methods for research may mean that alternatives could be available,” said Professor Thomas. “It is important that the necessity, usefulness and relevance of specific types of animal research are ascertained in each individual case.”

BBC News
June 20, 2006

Original web page at BBC News

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SIV has finally been tracked down in Wild West African chimps

Scientists have spotted the signs of an HIV-like virus in chimpanzees in southern Cameroon, confirming the long-held suspicion that these animals are a natural reservoir for the virus in the wild. The discovery bolsters the theory that the first people to contract HIV did so through contact with infected blood from wild chimps in the jungle, before eventually spreading the virus to nearby Kinshasa in the Democratic Republic of Congo and onwards from there.

Researchers led by Beatrice Hahn of the University of Alabama at Birmingham travelled to Cameroon to collect droppings from the chimpanzee subspecies Pan troglodytes troglodytes. The team knew that a few captive chimps of this subspecies have been found carrying a strain of simian immunodeficiency virus (SIV) almost identical to the HIV-1 strain, but it was not clear how these animals came to have the virus. Better evidence that these creatures were responsible for the human AIDS pandemic would come from tracking down a reservoir of the human-like SIV in wild chimps in west Africa. The team’s hopes of finding such a reservoir were high: a few years ago they found another version of SIV, one quite different from the human virus, in a different subspecies of wild chimp living in east Africa.

As hoped, analysis of the Cameroon samples revealed the presence of antibodies against human-like SIV and traces of the virus’ genetic sequence. On the basis of their samples, the researchers calculate that some 30-35% of chimpanzees are carriers. The team reports the findings in Science. The virus does not seem to cause any AIDS-like symptoms in the chimpanzees, says Hahn, as captive infected chimps do not seem to develop immune disease. “Lots of people are trying to find out why,” says Paul Sharp, a viral geneticist at the University of Nottingham, UK, who also worked on the study.

The virus probably got into humans as a result of bush meat hunting, Hahn suggests. “The most likely route, based on the biology of these viruses, is human exposure to infectious chimp blood or body fluids during hunting and butchering,” she says. The genetics of the wild chimp SIV are very close to the human virus. This suggests that humans contracted the virus directly from chimps, rather than both humans and chimps contracting it from monkeys, as some experts had previously suggested. It is unclear exactly how the virus arose in the chimps themselves, but it is probably derived from two viruses carried by monkey species on which the chimps prey, suggests Sharp.

Analysis of the path of the human pandemic has pinpointed Kinshasa as the epicentre of the outbreak. The first HIV-positive human blood was obtained here in 1959. The virus was almost certainly carried here by infected humans, says Sharp: “Chimps don’t walk the streets of Kinshasa.” The theory is supported by the fact that rivers, the primary transport routes through the dense West African jungle, provide an easy means of travelling from southern Cameroon to Kinshasa. Once there, the urban environment would have been far more conducive to the transmission of the virus between people. But it will be a difficult story to verify with certainty. “We’re talking about something thought to have happened more than 75 years ago,” he says. It seems to be largely a matter of chance that this strain became the one to terrorize the globe, says Sharp. HIV-2, thought to have come from sooty mangabey monkeys, also causes AIDS in humans, but this virus is confined almost entirely to West Africa.

Nature
June 6, 2006

Original web page at Nature

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Primate center research suggests multiple ‘body clocks’

Research conducted at Oregon Health & Science University suggests that contrary to popular belief, the body has more than one “body clock.” The previously known master body clock resides in a part of the brain called the suprachiasmatic nucleus (SCN). Researchers at OHSU’s Oregon National Primate Research Center (ONPRC) have now revealed the existence of a secondary clock-like mechanism associated with the adrenal gland. The research also suggests a high likelihood that additional clocks exist in the body. The study results are printed in the current edition of the journal Molecular Endocrinology.

“We’re all familiar with the idea that the body has a master clock that controls sleep-wake cycles. In fact, most of us have witnessed the impacts of this clock in the form of jet lag where it takes the body a number of days to adjust to a new time schedule following a long flight,” explained Henryk Urbanski, Ph.D., senior author of the study and a senior scientist at ONPRC. “Our latest research suggests that a separate but likely related clock resides in the adrenal gland. The adrenal gland is involved in several important body functions, such as body temperature regulation, metabolism, mood, stress response and reproduction. The research also suggests that other peripheral clocks reside throughout the body and that these clocks are perhaps interconnected.”

To conduct the research, scientists studied adrenal gland function in rhesus macaque monkeys which is very similar to human adrenal gland function. Specifically, researchers measured gene expression in the adrenal gland of monkeys during a 24-hour period (six times a day, four-hour intervals). In analyzing this information, researchers identified 322 genes in the adrenal gland with functions that varied rhythmically over a 24-hour period, meaning that each gene’s function peaked and diminished at the same time each day. Interestingly, the scientists also noted that a subgroup of these 322 genes also exist in the SCN — the home of the body’s master body clock. This suggests that the adrenal gland has its own timing mechanism that is related to, but separate from, the SCN body clock.

“Of course, different genes peaked in function at different times of the day,” explained Dario Lemos, an OHSU graduate student in the Urbanski lab and first author of the study. “For instance, genes controlling catecholamine secretion were more active in the day with function greatly decreasing at night. Catecholamines are involved in many important body functions, such as stress and mood.” This research provides important new information regarding the complex, rhythmic, 24-hour functions of the body. The research may also impact current therapies for a variety of diseases. For instance, data gathered in this study and future studies may suggest that certain therapies be delivered at certain times to synchronize with normal body functions controlled by body clocks.

“One example is testosterone replacement, a common treatment for certain disorders in males such as sexual dysfunction and depression,” explained Urbanski. “Patients receiving testosterone late in the day often complain of sleep loss. This is likely due to the fact that in healthy people, testosterone levels are lower in the afternoon and evening. As more data is gathered about body clock functions in our lab and others, we will likely learn of a specific window of time during the day where testosterone therapy is effective, but less disruptive for patients.”

Science Daily
June 6, 2006

Original web page at Science Daily

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T cell ‘brakes’ lost during human evolution

A significant difference between human and chimpanzee immune cells may provide clues in the search to understand the diverse array of human immune-related diseases. Researchers at the University of California, San Diego (UCSD) School of Medicine have uncovered a specific type of molecule expressed on non-human primate T cells, but not human T cells. T cells are important orchestrators of the immune system.

In a study to be published on-line in advance of publication in Proceedings of the National Academy of Sciences the week of May 1-5, UCSD researchers report that — unlike T cells from chimpanzees, bonobos, and gorillas (the “great apes” which are human’s closest evolutionary relatives) — human T cells lack expression of certain “Siglec” molecules. Siglecs are immune-dampening proteins that bind to sialic acids, the complex sugars found on the outside of cells. Siglec molecules seem to regulate T cell activation in chimpanzees by restricting the degree of signaling from the T cell receptor, which normally triggers the response of T cells in the immune system.

“Siglecs are like ‘brakes’ that can slow down the activation of an immune cell upon stimulation,” said Ajit Varki, M.D., UCSD Professor of Medicine and Cellular and Molecular Medicine and co-director of UCSD Glycobiology Research and Training Center. “During human evolution, we seem to have shut off these brakes on our T cells, allowing them to become hyper-active.” Human T cells respond much more robustly than chimpanzee cells do, a disparity that could be explained by the absence of human T cell Siglecs. The explanation for this human-specific evolutionary loss of Siglecs is currently unknown. The UCSD scientists speculate that this may have been due to a selective pressure by a microbe that once drove human ancestors to require a high level of T cell activation. Another possibility is that this phenotype was secondarily acquired, during the adjustment to the human-specific loss of the sialic acid Neu5Gc some three million years ago, and that the phenotype has been carried by all humans ever since.

The study raises warning flags about the stimulatory and potentially destructive potential of the absence of Siglec molecules in human T cells, compared to chimpanzees and other nonhuman primate counterparts. This may explain some major differences in susceptibility to certain diseases between humans and great apes. One example is the lack of progression to AIDS in the great majority of chimpanzees infected with HIV virus. It could also account for the rarity of T-cell mediated liver damage, such as chronic active hepatitis, cirrhosis and cancer, following Hepatitis B or C infection in chimpanzees. In addition, several other common human T cell-mediated diseases, including bronchial asthma, rheumatoid arthritis and type 1 diabetes, have, so far, not been reported in chimpanzees or other great apes.

The study suggests that the expression of Siglecs on chimpanzee T cells in essence puts the brakes on the cells during chronic HIV infection, preventing progression to AIDS in chimpanzees. In contrast, the onset of human AIDS occurs more rapidly due to the loss of T cells, which are essentially “unprotected” by the regulatory Siglecs. This study may also explain the severe human reactions observed in a recent clinical trial using a T cell activating anti-CD28 antibody produced by TeGenero, Inc. All six healthy volunteers who received doses at 500 times lower than what was tested in nonhuman primates became severely ill, requiring hospitalization.

“In retrospect, the absence of natural restrictions on activation, such as that provided by Siglecs, could have predicted this striking disparity between humans and nonhuman primates,” said Varki. The human volunteers could have experienced rapid activation of T cells and a resulting “cytokine storm.” The research team asked for a sample of the anti-CD28 antibody from TeGenero in order to test it on chimpanzee blood, but the company declined their request. While this family of molecules displays a striking difference between humans and nonhuman primates, the researchers point out that there may be other undiscovered factors that also contribute to the observed differences in immune function.

As our closest evolutionary cousins, chimpanzees share more than 99% identity in typical protein sequences with humans. For that reason, the common chimpanzee has long been assumed to be an effective animal model for human diseases. “In fact, chimpanzee diseases may be much more disparate from human diseases than previously envisioned,” said Varki. “The good news is that the loss of this brake system is not permanent, as we still have the Siglec genes in our genomes, and do continue to express them in other blood cell types,” said Varki. “It is reasonable to hope that drugs can be found to turn the Siglec brakes back on again in human T cells, to slow the T cells down when they become hyper-active and cause disease.”

Science Daily
May 23, 2006

Original web page at Science Daily

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Marburg and Ebola vaccine success in monkeys

A vaccine has shown effectiveness in treating deadly Marburg disease – a haemorrhagic fever closely related to the notorious Ebola virus – for which there is currently no cure. The study carried out in monkeys represents the first successful treatment of the disease, which causes internal bleeding at multiple sites and is usually fatal. The vaccine was first reported in June 2005, when Thomas Geisbert and colleagues at the US Army Medical Research Institute of Infectious Diseases, announced that they had successfully immunised a number of cynomolgus macaque monkeys that were then infected with Marburg. The same team have now taken the vaccine a step forward by testing it as a treatment after exposure to the virus, rather than before.

Five rhesus monkeys were infected with a high dose of Marburg virus and were then injected 20 to 30 minutes later with the vaccine. They all survived for at least 80 days. Three other monkeys that were also infected with the virus but not given a vaccine had all died by day 12 of the study. In a commentary accompanying the study, published in The Lancet, Stephan Becker from Germany’s Robert Koch Institute describes the work as good news for health workers who are in the front line against this highly contagious virus. But he cautions that a long road lies ahead before any Marburg vaccine can become commercially available. Since the disease is mercifully rare, it will be difficult to test a vaccine’s effectiveness among humans, he writes.

The vaccine comprises a harmless virus that has been genetically modified to express a surface glycoprotein from the Marburg virus. This primes the monkeys’ immune system against that pathogen. Marburg and Ebola are viruses that are passed between people through close contact with bodily fluids. They are lethal in more than 90% of cases. The world’s biggest outbreak of Marburg rampaged across Angola from October 2004 to July 2005, infecting 252 people, 227 of whom died, according to an official toll. Ten percent of the fatalities were health workers. It spreads through contact with blood, excrement, vomit, saliva, sweat and tears. The natural reservoirs for Ebola and Marburg are in Africa’s tropical forests, but the precise animal source remains unknown.

Source: The Lancet

New Scientist
May 9, 2006

Original web page at New Scientist

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Gene regulation separates humans from chimps

Scientists in the United States and Australia say changes in the gene expression, not just genes, is a big part of what separates humans from their nearest relatives. Gene expression is the process by which genes are turned on or off. Not all of the estimated 30,000 genes in humans are activated at the same time in every cell. “We think gene expression is a major part of what separates chimps and humans,” said Kevin White, an associate professor of genetics, ecology and evolution at Yale University in the United States.

White and researchers from the University of Chicago in Illinois and the Hall Institute in Parkville, Victoria in Australia looked at gene expression in humans, chimpanzees, orangutans and rhesus monkeys. They used new gene-array technology to compare the level of expression of 1,056 genes in the four species. “When we looked at gene expression, we found fairly small changes in 65 million years of macaque, orangutan and chimpanzee evolution,” said Dr Yoav Gilad of the University of Chicago, lead author of the study. But he said it was followed by quick changes in specific groups of genes known as transcription factors, which control the expression of other genes, since humans diverged from their ape ancestors during the last 5 million years.

“This rapid evolution in transcription factors occurred only in humans,” Gilad added in a statement. The research, which is published in the journal Nature, supports a 30-year-old hypothesis by scientists Mary-Claire King and Allan Wilson who suggested that key differences between humans and chimpanzees might be found in the way they express their genes. Until the mapping of the human genome and the development of gene array technology that allows for large-scale analysis of gene expression, it has not been possible to test the hypothesis. Gilad, White and their colleagues used samples of liver tissue from five adult males from each of the four species in their study. They found about 60 percent of the genes had consistent levels of expression in humans and the primates.

But genes for transcription factors were more likely to have changed their expression patterns than the genes they regulate. “Specifically in the human lineage the transcription factors are changing or evolving in their expression at a faster pace than in the other lineages, particularly as compared with chimps,” White said. The researchers do not know what caused the shift in gene expression in humans but they suspect it could be due to changes in the environment, the acquisition of fire and a preference for cooked food. They plan to use other types of tissue to look at large arrays of genes in future studies.

Reuters
March 28. 2006

Original web page at Reuters

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Great apes found to be rich in culture

The evidence is mounting that great apes are a cultured lot, researchers heard at the annual meeting of the American Association for the Advancement of Science (AAAS) in St. Louis this week. It is well established that apes are clever: gorillas lift electric wires with sticks to slip underneath; orang-utans can crack nuts open with rocks; and chimpanzees have been spotted elegantly sipping water from a sponge of crumpled leaves. But these tool-using apes also show signs of cultural traditions that vary from group to group, just as some customs are passed down from one generation to another in human societies. According to a trio of researchers at the AAAS, recent work has underscored the rich cultures of our nearest relatives.

In unpublished work, Tara Stoinski of the Dian Fossey Gorilla Fund in Atlanta surveyed zoos about their gorillas and turned up more than 40 cultural behaviours, such as hand clapping as an invitation to play, that varied from group to group. This hints that traditions are passed between apes. Even separate groups within the same zoo could vary, Stoinski found. Wild orang-utans also show cultural variation, says Carel van Schaik from the University of Switzerland in Zurich. In one case he has seen, the apes on one side of a river a different technique to remove seeds from a fruit to those across the river. “And up the river, there is no technique at all,” says van Schaik, who has identified roughly 40 cultural behaviours in orang-utans.

Van Schaik says he plans to use genetic tests to determine whether orang-utans that display the same behaviour are related. He hopes that these might also show how long ago some traditions originated. Chimps seem to be the most cultured nonhuman primates. Andrew Whiten from the University of St Andrews in Scotland says that researchers have found a huge range of chimp behaviours in the wild, including complex foraging techniques. Chimps even adopt what Whitten calls “fads and fashions” that only persist for a short time, such as a hand flapping behaviour that was hip in some young chimps for a while. The researchers say their findings will be useful in elucidating the origins of human cultures. “It helps to take some of the mystery out of cultural evolution in humans,” says Schaik. They add that an appreciation of culture in apes may encourage support for conservation. “The best we can do is engender respect and wonder for these animals that are so similar to us,” says Schaik.

Nature
March 14, 2006

Original web page at Nature

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Researchers assemble second non-human primate genome

A multi-center team has deposited the draft genome sequence of the rhesus macaque monkey into free public databases for use by the worldwide research community, the National Human Genome Research Institute (NHGRI), one of the National Institutes of Health (NIH), has announced. The rhesus macaque (Macaca mulatta) is the second non-human primate, after the chimpanzee (Pan troglodytes), to have its genome sequenced, and is the first of the Old World monkeys to have its DNA deciphered. Overall, the rhesus genome shares about 92 to 95 percent of its sequence with the human (Homo sapiens) and more than 98 percent with the chimpanzee. (Image courtesy of California National Primate Research Center / University of California, Davis)The rhesus macaque (Macaca mulatta) is the second non-human primate, after the chimpanzee (Pan troglodytes), to have its genome sequenced, and is the first of the Old World monkeys to have its DNA deciphered. Overall, the rhesus genome shares about 92 to 95 percent of its sequence with the human (Homo sapiens) and more than 98 percent with the chimpanzee. Consequently, the rhesus provides an ideal reference point for comparisons among the three closely related primates. Sequencing is also underway on the genomes of a number of other primates, including the orangutan, marmoset and gorilla.

The sequencing of the rhesus genome was conducted at the Baylor College of Medicine Human Genome Sequencing Center in Houston, the Genome Sequencing Center at Washington University in St. Louis and at the J. Craig Venter Institute in Rockville, Md., which are part of the NHGRI-supported Large-Scale Sequencing Research Network. The DNA samples used in the sequencing came from a female rhesus macaque at the Southwest Foundation for Biomedical Research in San Antonio.

Independent assemblies of the rhesus genome data were carried out at each of the three sequencing centers using different and complementary approaches. A team led by Granger Sutton, Ph.D., at the J. Craig Venter Institute, then joined the resulting data into a single, high-density draft, or “melded assembly.” This collaborative venture also made use of existing resources: the reference sequence of the human genome, published rhesus DNA mapping resources and the rhesus DNA fingerprint database from the Michael Smith Genome Sciences Center at the British Columbia Cancer Agency in Vancouver. The new, high-quality assembly, which covers 93 percent of the rhesus genome, will enable researchers to make evolutionary comparisons and accurate gene predictions for this important organism.

Because of its genetic, physiologic and metabolic similarities with humans, the rhesus macaque is the major, non-human primate used for the study of human disease, and also serves as an important system in drug development. Rhesus macaques are used for essential research in neuroscience, behavioral biology, reproductive physiology, endocrinology and cardiovascular studies. In addition, due to its response to the simian immunodeficiency virus (SIV), the rhesus is widely recognized as the best animal model for human immunodeficiency virus (HIV) infection. It also serves as a valuable model for studying other human infectious diseases and for vaccine research.

The availability of the rhesus genome sequence will facilitate study in these areas by enabling researchers to build a list of rhesus genes, as well as a list of differences between the rhesus, the chimpanzee and humans. A group of scientists has been organized to speed more detailed analyses of the rhesus data. The worldwide research community can access the sequence data through the following public databases and genome viewers: GenBank and Map Viewer at NIH’s National Center for Biotechnology Information (NCBI); EMBL Bank at the European Molecular Biology Laboratory’s Nucleotide Sequence Database; and the DNA Data Bank of Japan . The data can also be viewed through the UCSC Genome Browser at the University of California at Santa Cruz and the Ensembl Genome Browser at the Wellcome Trust Sanger Institute in Cambridge, England. Additional information about the rhesus sequence is available through the Human Genome Sequence Center at Baylor College of Medicine

Science Daily
February 28, 2006

Original web page at Science Daily

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Baboons in mourning seek comfort among friends

When Sylvia the baboon lost Sierra, her closest grooming partner and daughter, to a lion, she responded in a way that would be considered very human-like: she looked to friends for support. According to researchers from the University of Pennsylvania, baboons physiologically respond to bereavement in ways similar to humans, with an increase in stress hormones called glucocorticoids. Baboons can lower their glucocorticoid levels through friendly social contact, expanding their social network after the loss of specific close companions. “At the time of Sierra’s death, we considered Sylvia to be the queen of mean. She is a very high-ranking, 23 year-old monkey who was, at best, disdainful of females other than Sierra,” said Anne Engh, a postdoctoral researcher in Penn’s Department of Biology. “With Sierra gone, Sylvia experienced what could only really be described as depression, corresponding with an increase in her glucocorticoid levels.”

Engh works with Penn biologist Dorothy Cheney and Robert Seyfarth, a professor in Penn’s Department of Psychology. For the last 14 years, Cheney and Seyfarth have followed a troop of more than 80 free-ranging baboons in the Okavango Delta of Botswana. Their research explores the mechanisms that might be the basis of primate social relationships and how such relationships may have influenced the development of human social relationships, intelligence and language. To study the response of stress among baboons, Engh and her colleagues examined the glucocorticoid levels and grooming behavior of females in the troop to see how closely they resemble patterns seen in humans. Their findings were published in a recent article in the Proceedings of the Royal Society of Biological Sciences.

Grooming, a friendly behavior where baboons clean each other’s fur, is the primary means by which baboons strengthen social bonds. According to Engh, while the death of a close family member was clearly stressful over the short term, the females they studied appeared to compensate for this loss by broadening and strengthening their grooming networks. As they resumed grooming, their glucocorticoid levels returned to normal. “Without Sierra, Sylvia really had nobody else,” Engh said. “So great was her need for social bonding that Sylvia began grooming with a female of a much lower status, behavior that would otherwise be beneath her.”

Through her study, Engh was able to track patterns in stress of the female baboons over time through their glucocorticoid levels. Their stress levels increased most often during events when their lives, the lives of their offspring and their social rankings were at risk. The leading cause of death among adult baboons is predation, usually from leopards and lions. The stress levels of female baboons increased most noticeably when a predator killed a close companion, such as a grooming partner or offspring. If they merely witness another baboon die they do not become as agitated. “Our findings do not necessarily suggest that baboons experience grief like humans do, but they do offer evidence of the importance of social bonds amongst baboons,” Engh said. “Like humans, baboons seem to rely on friendly relationships to help them cope with stressful situations.

Science Daily Health & Medicine
February 28, 2006

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Humans have a strong desire to help each other, but is spite also part of the human condition?

In a study published in the Proceedings of the Royal Academy (January 17, 2006), Keith Jensen and colleagues from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany looks at altruism and spite in our close cousin; the chimpanzee. In Jensen’s study, chimpanzees from the Wolfgang Koehler Primate Research Centre in Leipzig were given a choice; by pulling on a rope they could either deliver food to another chimpanzee or they could deliver it to an empty room. In both cases, the chimpanzee pulling the rope did not receive any food itself. Contrary to initial expectations the chimpanzees behaved neither altruistic nor spiteful. According to the researchers, both characteristics therefore seem to be human-specific.

An altruistic chimpanzee would give food to its neighbour, despite the effort in pulling the food, and a spiteful chimpanzee would prevent its neighbour from having the food by delivering it to the empty room. ‘I predicted chimps would be spiteful. I thought if they knew they couldn’t have the food, they wouldn’t let anyone else have it.’ Jensen found that half the time, the chimpanzees did nothing. A quarter of the time they delivered food to their neighbour, then a quarter of the time to the empty room. This demonstrated neither altruism nor spite. ‘They didn’t seem to care about the other guy one way or the other. All that concerned them was getting the food and they were completely focused on that. Even when they knew they couldn’t have the food, they didn’t help the other chimp but they weren’t spiteful either.’

In contrast, humans are obviously altruistic. We give blood, we donate money to charity, and we volunteer to help strangers. This kind of altruism has never been demonstrated in any other animal except for humans and some believe it is one of the characteristics that makes us human. But Jensen says spite is just as important. As a form of punishment, spite can encourage cooperative behaviour by penalising cheaters. ‘Punishing others is usually costly to yourself, whether that’s the taxpayer or the lawmakers but punishment is still a natural part of modern society. We punish theft, murder and countless other crimes to keep the fabric of society together. Perhaps human society is where it is today because spite exists and there is a mechanism to punish cheaters.’

If altruism and spite are unique to humans and are not present in chimpanzees, then it is likely that these characteristics have arisen in the last 6 million years since humans and chimpanzees shared a common ancestor. Humans’ intense regard for each other, either positive or negative, may have made an important contribution to our ability to cooperate, our sense of fairness, and the morality that defines today’s society.

Science Daily
February 14, 2006

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Performing monkeys in Asia carry viruses that could jump species to humans

Some urban performing monkeys in Indonesia are carrying several retroviruses that are capable of infecting people, according to a new study led by University of Washington researchers. The results indicate that contact with performing monkeys, which is common in many Asian countries, could represent a little-known path for viruses to jump the species barrier from monkeys to humans and eventually cause human disease. Performing monkeys are animals that are trained to produce tricks in public. While scientists have conducted extensive research on primate-to-human viral transmission in Africa, where they believe HIV originated, few have researched this topic in Asia.

“People aren’t looking at Asia, and they need to do so, because viruses are emerging on that continent,” explained Dr. Lisa Jones-Engel, leader of the study and a research scientist in the Division of International Programs at the UW’s Washington National Primate Research Center. “There is a large, diverse population of primates there, and a huge human population in dense urban centers, so there’s the potential for viral transmission across the species barrier.”

The study’s authors are urging more research on the different settings in Asia where people have contact with non-human primates – zoos, animal markets, monkey forests, pet ownership, and urban street performances. Most previous research on viral transmission has focused on bushmeat hunting and consumption, a practice in which local residents hunt wild monkeys for food. HIV, the virus that causes AIDS in humans, is believed to have originated as a primate virus and jumped the species barrier to humans when African bushmeat hunters came into contact with blood from infected animals.

However, in Asia other forms of primate/human contact, among them urban monkey performances, may be more prevalent than bushmeat hunting. Asia has a long history of performing monkeys, and initial studies indicate that the performances can include very close, physical contact between the animals and human spectators – monkeys crawling on people, for instance. Such contact might increase the risk of a bite, scratch, or other interaction that could lead to exposure to monkey body fluids. “The risk of viral transmission in this context is unclear,” said Dr. Michael Schillaci, professor of social sciences at the University of Toronto at Scarborough and lead author on the study. “But the contact here can be very intense.”

Also troubling are the animal markets where many performing monkeys are acquired by their trainers. The markets typically bring together many different species of wild monkeys, as well as many other types of animals, in very close, unnatural quarters and unsanitary conditions. “The market is a condensed area for mixing species and pathogens,” explained Dr. Gregory Engel, an attending physician at Swedish/Providence Hospital in Seattle, Wash., a clinical instructor of family medicine at the UW, and a co-author on the study. “The animals may be sick or in bad shape there, and they’re mixed with other animals that potentially could have pathogens, and then they’re put into contact with a dense human population.”

In this study, the researchers drew blood from 20 urban performing macaques in Jakarta, Indonesia, and tested those samples for various simian viruses. They found that about half of the macaques tested positive for simian foamy virus (SFV), a primate retrovirus that so far has not been shown to cause disease in humans, but that has been detected in other monkey-human interaction settings in Asia. Two of the monkeys tested positive for simian retrovirus (SRV), which, though it has been shown to infect humans in a laboratory setting, has yet to be associated with any disease in humans. However, both SRV and SFV are retroviruses, which are typically slow-acting in their host, so it could be many years before physicians know the effects of those virus exposures. One monkey tested positive for simian T-cell lymphotropic virus (STLV), which is believed to be the primate ancestor to the human version of the virus, HTLV, a known cause of T-cell leukemia in people. One macaque tested positive for herpes B virus, also known as CHV-1, which rarely infects humans, but, in the 40 known human cases, was associated with an 80 percent fatality rate.

The researchers still do not know the prevalence of such simian viruses across larger urban performing monkey populations in Indonesia, or elsewhere in Asia. Urban performing monkeys can be found in India, Pakistan, Thailand, Vietnam, China, Japan and Korea. They hope to learn more about the risk of primate to human viral transmission in future studies of owners and their monkeys. However, they urge people to take precautions around performing monkeys, by preventing the animals from climbing on them and by keeping food away from the macaques. Such precautions can help reduce the risk of bites and scratches from the monkeys.

Science Daily
January 3, 2006

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New procedure reveals the secrets of the brain

Scientists from the MPI for Biological Cybernetics in Tübingen have developed a new procedure which accurately maps the activity in primate brains by means of the BOLD-Signal (Blood Oxygen Level Dependent Signal). The combination of electrical microstimulation and FMRT promises substantially more precise insights into the functional organisation or the brain and its circuitry. (Neuron, December 22, 2005). Activity patterns in the brain elicited by electrical microstimulation are observed around the electrode and in other functionally connected visual areas. Functional magnetic resonance imaging was used to measure activation. Over the last two centuries electrical microstimulation has been often used to demonstrate causal links between neural activity and specific behaviors or cognitive functions. It has also been used successfully for the treatment of several neurological disorders, most notably, Parkinson’s disease. However, to understand the mechanisms by which electrical microstimulation can cause alternations in behaviors and cognitive functions it is imperative to characterize the cortical activity patterns that are elicited by stimulation locally around the electrode and in other functionally connected areas.

To this end, in a new study published in the December, 2005, issue of Neuron, Andreas S. Tolias and Fahad Sultan, under the guidance of Prof. Nikos K. Logothetis from the Max Planck Institute for Biological Cybernetics in Tübingen, have for the first time developed a technique to record brain activity using the blood oxygen level dependent (BOLD) signal while applying electrical microstimulation to the primate brain. They found that the spread of activity around the electrode in macaque area V1 is larger than expected from calculations based on passive spread of current and therefore may reflect functional spread by way of horizontal connections. Consistent with this functional transsynaptic spread they also obtained activation in expected projection sites in extrastriate visual areas demonstrating the utility of their technique in uncovering in vivo functional connectivity maps. Using the microstimulation/MRI technique in conscious, alert primates holds great promise for determining the causal relationships between activation patterns across distributed neuronal circuits and specific behaviors. Finally, this method could also proof useful in understanding and optimising the method of intra-cranial electrical stimulation in the treatment of neurological diseases.

Science Daily
January 3, 2006

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The brain needs the middle ear to track depth

When you jaywalk, your ability to keep track of that oncoming truck despite your constantly changing position can be a lifesaver. But scientists do not understand how such constant updating of depth and distance takes place, suspecting that the brain receives information not just from the eye but also from the motion-detecting vestibular system in the middle ear. In studies with monkeys reported in the October 6, 2005, issue of Neuron, Nuo Li and Dora Angelaki of Washington University School of Medicine in St. Louis have demonstrated how such depth motion is updated and strongly implicated the vestibular system in that process.

In their experiments, the researchers trained the monkeys to perform memory-guided eye movements. The animals were first shown a light a fixed distance away from their head. Then the researchers flashed one of eight other, closer “world-fixed” target lights. Next, with the room lights turned off, the monkeys were moved either forward or backward and the fixed-distance light flashed, signaling the monkeys that they should look at where they remembered the world-fixed light had flashed. Finally, the room lights and target light were turned on, so the monkey could make any corrective eye movement to the re-lit target. For comparison, the researchers also conducted experiments in which the monkeys were not moved. Such an experimental design using passive motion enabled the researchers to study depth-tracking in the absence of any clues the monkeys might have gleaned from their own motor movements–leaving vestibular system as the most likely source of information.

Finally, the researchers eliminated the vestibular systems in two of the monkeys and performed the same eye-movement experiments. They found that the eye motion of monkeys in the first experiments indicated that they were clearly able to update their perception of the depth of the target, even in the absence of information from their own motor movements. By contrast, the monkeys that lacked vestibular systems showed compromised ability in the task. “These results demonstrate not only that monkeys can update retinal disparity information but also that intact vestibular motion cues are critical in reconstructing three-dimensional visual space during motion in depth,” concluded Li and Angelaki.

Science Daily
November 8, 2005

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Human Y chromosome stays intact while chimp Y loses genes

The human and the chimpanzee Y chromosomes went their separate ways approximately 6 million years ago. But ever since this evolutionary parting, these two chromosomes have experienced different fates, new research indicates. Since the time of the divergence of the X and Y chromosome roughly 300 million years ago, the Y chromosome has lost nearly all of its unpartnered genes. This has led some to predict that, given a constant rate of decay, the Y chromosome will be completely devoid of functional genes in 10 million years. The chimpanzee ancestors diverged from ours about 6 million years ago. By comparing the gene catalog of the chimpanzee Y chromosome to ours, it is clear that the human Y chromosome has not lost any of its unpartnered genes in the past 6 million years. While the human Y has maintained its count of roughly 27 genes and gene families over the last 6 million years, some of these same genes on the chimp Y have mutated and gradually become inactive. The authors speculate that one likely reason for such disparity is due to chimpanzee mating habits.

“Contrary to the dire predictions that have become popular over the last decade, the sky is *not* falling on the Y,” says Whitehead Member and Howard Hughes Medical Institute investigator David Page, senior author on the study that appeared in the September 1 issue of the journal Nature. “This research clearly demonstrates that natural selection has effectively preserved regions of the Y chromosome that have no mechanisms with which to repair damaged genes.” For many years, it’s been assumed that the Y chromosome is headed for extinction because, unlike other chromosomes, it has no genetic “mate” with which to swap genes. In 2003, Page published a landmark paper in Nature challenging that claim by demonstrating how a certain region of the Y chromosome possessed a unique mechanism for repairing mutated genes.

Through sequencing the Y, the Page lab and collaborators at Washington University School of Medicine in St. Louis discovered that many of its genes were located in palindromes–long stretches of DNA letters that read the same forwards and backwards. By folding into a hairpin, the authors suggested, a gene might then swap the appropriate genetic material with itself. This demonstrated a process for the Y chromosome to maintain its integrity despite lacking a mate. However, there is another region of the Y, called the “X-degenerate” region, where the genes are not situated in palindromes.

“The genes in the palindrome region are primarily sperm-producing genes, and most other genes unique to the Y aren’t located there,” says Jennifer Hughes, a postdoctoral scientist in Page’s lab and first author on the paper. These other genes have no obvious means for self-repair. Because of this, many proponents of the “Y’s demise” theory remained undaunted. Once again collaborating with Richard Wilson from the Washington University School of Medicine in St. Louis Missouri, Page and his research team sequenced this X-degenerate region of the chimpanzee Y chromosome and compared it to the human Y. “We were looking for any evidence that the human Y has lost genes since parting ways with the chimp,” says Hughes. “Had we found active genes on the chimp Y that had become inactive on the human, that would be the smoking gun. But we didn’t find any such evidence. In fact, we found the opposite.”

On the chimp Y, five genes have suffered mutations that rendered them inactive. On the human Y, those same genes continue to function perfectly. “So then,” says Hughes, “even though the Y has lost many genes since its origin about 300 million years ago, it’s been holding steady in humans for the last 6 million years.” In other words, if the one region of the Y can depend on itself for survival, the other region has found a friend in evolution. “We now see that natural selection *is* working to conserve this unpartnered region of the Y,” says Page, who is also a professor of biology at MIT. “If mutations do occur in any of these genes, they don’t seem to pass on in the lineage. This is a clear example of how evolution is not just about moving ahead, it’s also about not falling behind.”

Fortunately for the primate world, male chimps, just like male humans, are probably not bound for early extinction. Those genes in the X-degenerate region are what scientists call “housekeeping” genes, meaning that they are active in most cells in the body and don’t carry out any male-specific functions. Page and his team speculate that the loss of genes on the chimpanzee Y may be due to the chimp’s mating habits. Both male and female chimps engage with multiple partners when they mate. This gives a strong selective pressure on those genes that produce sperm. Conversely, it puts less pressure on evolution to preserve those genes on the Y whose functions have nothing to do with reproduction. Because humans historically have been largely monogamous, our Y chromosomes have been spared such selective-pressure imbalance. “Of course,” acknowledges Page, “this is a hypothesis that we have no way to scientifically prove or disprove. However, we believe it’s currently the best explanation.”

Science Daily
October 11, 2005

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The chimpanzee genome is unveiled

The chimp genome sequence, which consists of 2.8 billion pairs of DNA letters, will not only tell us much about chimps but a comparison with the human genome will also teach us a great deal about ourselves. The major accomplishment is that we now have a catalogue of the genetic differences between humans and chimps,” says lead author, Tarjei Mikkelsen of the Broad Institute in Cambridge, Massachusetts, US. In keeping with previous studies comparing much smaller portions of the chimp and human genomes, the new comparison shows incredible similarity between the genomes. The average number of protein-changing mutations per gene is just two, and 29% of human genes are absolutely identical. What is more, only a handful of genes present in humans are absent or partially deleted in chimps. But the degree of genome similarity alone is far from the whole story. For example, the mouse species Mus musculus and Mus spretus have genomes that differ from each other to a similar degree and yet they appear far more similar than chimps and humans.

Domestic dogs, however, vary wildly in appearance as a result of selective breeding and yet their genome sequences are 99.85% similar. So most of the differences between chimp and human genomes will turn out to be neither beneficial nor detrimental, in evolutionary terms. The real challenge then will be finding the changes that played a major role in the evolution of chimps and humans since the two lineages split, 5 to 8 million years ago. Nothing obvious has leapt out of the initial analysis. “From this study, there’s no silver bullet of what makes chimps chimps and humans humans,” says Evan Eichler of the University of Washington at Seattle, US.

Comparing the two genomes has thrown up numerous candidates for what makes humans different though. One such set came by comparing 13,454 specific genes in the chimp and human genomes, looking for signs of rapid evolution. For each gene, the researchers compared the number of single letter mutations that alter the encoded protein versus silent mutations that have no effect. Silent mutations are possible because most amino acids are coded by more than one 3 letter DNA ‘word’ – for example, proline is coded by CCU, CCC, CCA, and CCG, so a change at the third position makes no difference to the protein. Comparing the two types of mutations allowed the team to spot genes that have had changes favoured by natural selection while taking into account the background mutation rate. And 585 of the genes studied in this set – many involved in immunity to infections and reproduction – had more protein-altering mutations than silent ones. Mikkelsen believes these will be a good place to look for genes that make humans different from chimps.

But comparing genome sequences can only tell scientists so much. Now begins the methodical job of homing in on the promising parts of the sequence and identifying the differences that count. “This is best viewed as an exciting starting point,” says Simon Fisher at the Wellcome Trust Centre for Human Genetics at Oxford University, US. “In the same way that knowledge of our own genome sequence has not automatically led to a full understanding of human biology, so the decoding of other primate genomes will not, by itself, reveal exactly what sets us apart.” But he admits: “Coming face to face with the details of evolution is really spectacular.”

Source: Nature (vol 437, p69)

New Scientist
September 27, 2005

Original web page at New Scientist

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Monkey brain’s ‘pitch center’ discovered

Johns Hopkins University scientists have discovered a discrete region of the monkey brain that processes pitch — the relative high and low points of sound. By recording the activity of individual brain cells as monkeys listened to musical notes, the scientists identified single neurons that recognize a middle-C as a middle-C even when played by two different instruments. “Pitch perception is a basic function of human and animal auditory systems, yet its source has remained elusive to researchers for decades,” said Xiaoqin Wang, associate professor of biomedical engineering and neuroscience. “The discovery of a pitch-processing area in the brain solves an age-old mystery of auditory research.”

Wang said pitch’s importance to humans is found in facilitating the ability to follow a sequence of sounds recognized as “melodic” and combinations of sounds identified as harmony. As a result, pitch gives meaning to the patterns, tones and emotional content of speech. The researchers say given the similarities between monkeys and man, humans may have a similar pitch-processing region in the brain. Such a discovery might help people with hearing and speech problems.

Source: Nature

Science Daily
September 27, 2005

Original web page at Science Daily

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Chimp papers by the barrel

A detailed comparison of the human and chimpanzee genomes reveals that some genes coding for transcriptional regulators may be evolving faster in humans, an international research consortium comprising 67 authors reports today in Nature. The paper, arriving a year and a half after the chimp draft, is accompanied by a cluster of studies in Science, Genome Research, and Nature that use this powerful comparative tool to assess gene-expression patterns across different organs, test a prevailing theory about Y-chromosome evolution, and find elements and mediators of genomic variation. The sequence should expand the scope of chimpanzee research say those involved, and may aid in investigations into what makes humans human. “The chimp genome is exciting because it gives us the raw material to ask that question,” said Michael Eisen at the University of California, Berkeley, who did not participate in these studies.

Chimps and humans split from a common ancestor 6 million years ago; the comparison shows that human and chimpanzee genomes are 96% identical, but it is the differences between the species–as many as 3 million of which fall in functional areas of the genomes–on which research now focuses. According to the main study, the catalog of genetic differences includes about 35 million single-nucleotide changes, 5 million insertion/deletion events, and a number of other chromosomal rearrangements. Members of the consortium assessed deviations from expected mutation patterns. In the human genome, they found evidence of selective sweeps in the past quarter million years in regions containing genes like FOXP2—which has been associated with speech acquisition in humans.

Some genes are evolving more rapidly in humans than in chimps, particularly transcriptional regulators, according to the paper. They also found that both humans and chimps have acquired more potentially deleterious mutations than mice, rats, and other rodents—perhaps making them better able to adapt to a changing environment.

In another study, Wolfgang Enard and colleagues at the Max-Planck Institute for Evolutionary Anthropology in Germany looked at protein sequences and expression patterns for genes in various chimp and human tissues and found a gradation of selective constraints on the organs they studied. While the brain showed the fewest differences between the species, genes active in the brain have accumulated more changes in humans than in chimpanzees. The researchers also found evidence of positive selection in human evolution for X-chromosomal genes expressed in testis. According to Enard, this is probably because “it’s so directly relevant for reproduction. If I am a sperm and I have a mutation that lets me divide faster…it will have a huge effect on my distribution,” he told The Scientist.

A group at the Whitehead Institute, which had previously sequenced the human Y chromosome, compared it to the chimp’s Y-chromosome sequence to assess the widely held “impending demise” hypothesis: that the 16 unique genes on the human Y chromosome which don’t have gene-conversion partners, will completely disappear in the next 10,000 years. Contrary to the hypothesis, they found that all of the genes were actually maintained in humans since they diverged from chimps, but that five of them had been inactivated in the chimp’s Y chromosome.

For our more “promiscuous” cousins, “sperm competition is intense,” said Jennifer Hughes, a postdoctoral scientist at the Whitehead Institute and first author on the study. So her group speculated that the strong selective pressure on the Y-linked genes coding for such male fertility traits–which are found in palindromes that give the genes pairing partners–outweighs the drive to maintain those 16 “partnerless” genes in chimpanzees. Hughes said these unique genes are “civilian casualties in the sperm wars.” She told The Scientist, “We’re hoping this will put the [impending] demise theory to rest once and for all.”

Two other studies looked more at elements of genomewide variation. A team led by Evan Eichler at the University of Washington School of Medicine in Seattle showed that segmental duplications have a much greater impact on genome differences between species than previously realized. They found that these “large-scale genetic events” altered about 2.7% of the genome, while the more commonly studied single base-pair changes account for changing 1.2% of the genome. The researchers found that several duplicated genes associated with developmental disorders in humans were single-copy in the chimp genome, suggesting that the chimpanzees may not be disposed to the same diseases. They also connected much of the species-specific duplications to differences in gene expression.

A study by researchers in Canada and Sweden compared human and chimp genomes with that of the more primitive Rhesus monkey and found that retroelements, or “jumping genes,” have been deleted in the course of evolution; they also found a possible mediator of these retroelement deletions and of thousands of insertion-deletion sequence differences between human and chimp genomes: short identical sequences flanking deleted regions.

The Scientist
September 27, 2005

Original web page at The Scientist

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Cracking the perception code

The brain may interpret the information it receives from sensory neurons using a code more complicated than scientists previously thought, according to new research from the National Autonomous University of Mexico and Cold Spring Harbor Laboratory. By studying how monkeys perceive a vibrating object when it touches the skin, scientists found that changes in an animal’s attention over time influence how a sensory signal is interpreted.

Neuroscientists already knew that touching the skin with a vibrating object causes specialized sensory neurons in the brain to fire, and that firing of these neurons, which are found in a region of the brain known as the primary somatosensory cortex, is directly related to monkeys’ ability to tell how fast something is vibrating, Romo said. But the neurons’ firing patterns are complex, and it’s been tricky to tease out “which component of the neuronal activity was more likely associated with behavioral performance,” he explained. Theoretically, there are many ways in which neurons could relay information about stimulus frequency, Romo said. Frequency information might be encoded in the time between consecutive neuronal firings, the overall rate of firing, or the number of times a neuron fires.

To distinguish among these possibilities, Romo and his colleagues designed an experiment in which they touched the monkeys’ fingertips with a vibrating but painless probe for varying lengths of time. The monkeys were first taught to respond to varying vibration frequencies; in a training session, the scientists touched the monkeys twice in a row, with the probe vibrating at a different frequency each time. The monkeys signaled to the experimenters which stimulus was vibrating faster, and, when they were correct, they were rewarded with a treat.

The standard stimulus that the scientists trained the monkeys to respond to lasted 500 milliseconds (half a second). They found that when they used a stimulus that lasted 750 milliseconds instead, the monkeys consistently thought the probe was vibrating with a higher frequency than it actually was. The same thing happened in reverse; if a stimulus was given for only 250 milliseconds, the monkeys thought it was vibrating at a lower frequency. The effect was stronger for the shortened stimulus than for the lengthened stimulus, Romo noted.

Based on this experiment, it seemed most likely that the monkeys were determining the vibration frequency by the number of times the neurons fired, Romo said, since the firing rate and time between firings wouldn’t change just because the stimulus duration changed. The scientists knew they hadn’t quite cracked the neural code, though, because the magnitude effects weren’t right; the monkeys thought that a stimulus that was 50 percent shorter was vibrating at just a slightly lower frequency than it was–not 50 percent lower.

To find the cause of this discrepancy, they recorded electrical activity in single neurons of the primary somatosensory cortex. Since the shortened stimulus had produced a greater effect than the lengthened stimulus, the researchers wondered if the first part of the response might be more significant in determining vibration frequency. They explored two possible mechanisms of action: the neural firing response could adapt to the stimulus over time, making the neurons more sensitive at the beginning than at the end, or a perceptual process after neuronal firing could give more subjective weight to the beginning of the response.

Looking at the electrical responses from single neurons, Romo and his colleagues determined that, if all the neuronal firings were treated equally, these responses could not explain the monkeys’ perception of the signal. If the researchers assumed that the monkeys paid more attention to the beginning of the response, however, the neural activity perfectly explained the monkeys’ errors when judging different durations of stimuli.

Romo suggested that the best explanation for the behavioral data was to assume that the monkeys pay the most attention to the first 250 milliseconds of neural firing, and that their attention falls off exponentially from there. The longer the stimulus, the less important additional neuronal firings become to the monkeys’ perception of how fast the stimulus is vibrating, even though they continue to pay some attention throughout.

Figuring out how the brain codes sensory information into neuronal firing and how the firing patterns are interpreted by perceptual areas of the brain is a huge challenge in neurophysiology, one that’s often overlooked, said Romo. “The neuronal correlates reported in most of the neurophysiological studies in the different sensory modalities simply do not pay attention to this,” he noted. “They assume that variation in firing rate is enough as a measure.”

Source: Howard Hughes Medical Institute

Bio. com
August 16, 2005

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Primate virus jumps species barrier to humans for first time in Asia

Scientists have identified the first reported case in Asia of primate-to-human transmission of simian foamy virus (SFV), a retrovirus found in macaques and other primates that so far has not been shown to cause disease in humans. The transmission of the virus from a monkey to a human took place at a monkey temple in Bali, Indonesia, the researchers report in the July issue of the journal Emerging Infectious Diseases. Even though this particular virus jumping to humans may not prove dangerous, the scientists warn that the dense human and primate populations in Asia could lead to other primate-borne viruses jumping the species barrier and causing human disease. “The issue of primate-to-human viral transmission has been studied extensively in Africa, largely because that is where HIV originated,” explains Dr. Lisa Jones-Engel, lead author of the study and a research scientist in the Division of International Programs at the Washington National Primate Research Center. “But there has not been much work on the topic in Asia, which has huge primate diversity and large human populations.”

Jones-Engel and her co-authors also argue for more research on diverse contexts of human-primate contact. The vast majority of previous viral transmission research focused on bushmeat hunting and consumption, a practice in which local residents hunt monkeys for food. HIV, the virus that causes AIDS in humans, is believed to have originated as simian immunodeficiency virus (SIV), and jumped the species barrier to humans when African bushmeat hunters came into contact with blood from infected animals. Though bushmeat hunting and consumption may be a significant factor in viral transmission in Africa, Jones-Engel says, people in Asia have many other contexts in which they come into contact with primates, including animal markets, primate pet ownership, urban performing primates, and zoos. In addition, monkeys are significant symbols in both Buddhism and Hinduism, and monkey temples – places of religious worship that have become refuges for populations of primates – are common throughout much of South and Southeast Asia. In these areas, protected macaque populations have thrived alongside dense human settlement for centuries.

On the island of Bali alone, there are more than 40 such temples, which are frequented by tourists from around the world. About 700,000 international tourists visit the island’s four main monkey temples every year. Temple workers and people who live near the temples also have a great deal of contact with monkeys at the religious sites. “In Asia, the amount of contact between humans and primates in temple settings dwarfs the contact due to bushmeat hunting,” says Jones-Engel. For this study, the researchers tested blood samples from 82 people who work in or around a temple in Bali, as well as samples from macaques in the area. They found antibodies for simian foamy virus in the blood of one 47-year-old farmer who visited the temple every day. They confirmed the tests by performing a DNA analysis of the man’s blood, and found that the SFV strain he carried was the same strain found in the temple’s macaques. The man denied owning a monkey as a pet, or hunting monkeys for food. He had been bitten once and scratched more than once by the temple’s macaques.

Researchers still don’t know the long-term effects of SFV on humans – there are about 40 known cases of people being infected, through laboratory or zoo contact, or through bushmeat hunting in Africa. There are no known cases of human disease yet. However, Jones-Engel and her fellow researchers warn that there are other primate viruses known to be harmful that could jump the species barrier. They don’t want people to be afraid of coming in contact with macaques or other primates, but they do urge people to be cautious and careful when interacting with monkeys. Feeding the animals, or even carrying food into a temple, can greatly increase the risk of a bite or scratch, which can lead to transmission of infection. Visitors occasionally engage in other risky behavior, such as touching animals or trying to hold baby monkeys. Limiting such behavior can reduce the risk of bites and scratches.

“If you look at free-ranging monkeys in Singapore’s nature reserves, you see that feeding by visitors is not allowed, and it is actively discouraged,” says Gregory Engel, an attending physician at Swedish/Providence Hospital in Seattle, Wash., a clinical instructor of family medicine at the University of Washington, and a co-author on the study. “Interspecies interaction there is very different, and rates of human-monkey contact are much lower.” Limiting dangerous contact between primates and humans can have other benefits, as well, such as reducing the transmission of human infections to monkeys. Human measles, for instance, can cause disease in monkeys and can even kill them. Other primate species have already seen significant population losses because of infection by human illnesses.

Source: University of Washington

Bio.com
August 2, 2005

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Dietary supplementation of docosahexaenoic acid and arachidonic acid in baboon neonate central nervous system

Docosahexaenoic acid (DHA) and arachidonic acid (ARA) are major components of the cerebral cortex and visual system, where they play a critical role in neural development. We quantitatively mapped fatty acids in 26 regions of the four-week-old breastfed baboon CNS, and studied the influence of dietary DHA and ARA supplementation and prematurity on CNS DHA and ARA concentrations. Baboons were randomized to 5 groups, a breastfed (B) and four formula-fed groups: term, no DHA/ARA (T-); term, DHA/ARA supplemented (T+); preterm, no DHA/ARA (P-); preterm, DHA/ARA supplemented (P+). At four weeks adjusted age, brains were dissected and total fatty acids analyzed by gas chromatography and mass spectrometry.

DHA and ARA are rich in many more structures than previously reported. They are most concentrated in structures local to the brain stem and diencephalon, particularly the basal ganglia, limbic regions, thalamus, and midbrain, and comparatively lower in white matter. Dietary supplementation increased DHA in all structures but had little influence on ARA concentrations. Supplementation restored DHA concentrations to levels of breastfed neonates in all regions except the cerebral cortex and cerebellum. Prematurity per se did not exert a strong influence on DHA or ARA concentrations.

Conclusions: 1) DHA and ARA are found at high concentration throughout the primate CNS, particularly in gray matter such as basal ganglia, 2) DHA concentrations drop across most CNS structures in neonates consuming formulas with no DHA, however ARA levels are relatively immune to ARA in the diet, 3) supplementation of infant formula is effective at restoring DHA concentration in structures other than the cerebral cortex. These results will be useful as a guide to future investigations of CNS function in the absence of dietary DHA and ARA.

BioMed Central
July 19, 2005

Original web page at BioMed Central

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Orang-utans killed for illegal trade

Around 1000 orang-utans are being killed each year so that their babies can be traded as pets, leaving the primate species on the brink of survival, the WWF warns in a new report. The orang-utan – meaning “man of the forest” in Malay – is native to the tropical rainforests of Sumatra and Borneo. They are already under severe threat due to intensive logging of their habitat – over 90% of the species were wiped out during the last century.

Orang-utans are now the most expensive primates for sale in Indonesian markets – the babies are kept as household status symbols or traded for use in the entertainment industry. Once they reach adulthood, many are killed or abandoned, says the report. It has been illegal to hunt or trade in orang-utans since 1931, but the study by WWF and TRAFFIC, the wildlife trade monitoring network, discovered that fewer than 10% of people found in illegal possession of the apes were prosecuted.

Christian Thompson, species officer for WWF, called on the Indonesian judiciary and police to enforce the existing laws to protect the remaining 40,000 to 55,000 orang-utans. “The solutions are clear – we need better enforcement of the law to protect orang-utans and gibbons from being captured and traded illegally. Bird markets need to be monitored stringently, and a wide-scale education campaign needs to be launched in Indonesia to raise awareness about this appalling trade,” he says.

New Scientist
July 5, 2005

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Honking monkey discovered in Africa

To the ears of Trevor Jones, the calls made by geese and dogs will never sound the same again. Combining the two noises produces something similar to the unique ‘honk-bark’ of a monkey species discovered last year in Tanzania by two groups of wildlife biologists. Jones, who leads a team at the Udzungwa Mountains National Park in Tanzania, and Tim Davenport, a biologist at the Wildlife Conservation Society in Mbeya, discovered the species almost simultaneously on mountain ranges some 370 kilometres apart.

The researchers classified the animal as Lophocebus kipunji and gave it the common name ‘highland mangabey’. These medium-sized monkeys dwell in trees and have a black face with long whiskers. But what caught the scientists most off guard was the distinctive noise that they make. The two highland mangabey populations are separated by dry bush.
Because the monkeys can only move and thrive in forest environments, this is evidence that forest probably connected the two mountain areas in the past. “At some point the populations had a common ancestor in one site,” says Jones. The teams report their discovery in this week’s Science.

But the mangabeys are already threatened, says Davenport. Land development threatens the small remaining forest where highland mangabeys can survive. Davenport and his colleagues estimate that fewer than 1,000 of these monkeys exist and have recommended that the species be classified as critically endangered. “I would say that habitat loss is probably the major contributing factor,” he says. The chances of finding other, undiscovered populations of highland mangabeys are slim. “It’s possible, but personally I think it’s unlikely,” Jones admits. “Most of the mountain forest of southern Tanzania has already been surveyed.”

Because there are so few highland mangabeys left, the researchers have chosen not to capture any of them. But they do hope to obtain DNA samples in the wild to analyse how closely related the animals are to other mangabey species. Colin Groves, a taxonomist at the Australian National University in Canberra, stresses that more monkey species may yet be discovered. “The find indicates that there is a lot that we don’t know even about comparatively large mammals,” he says. There are already about 90 species of monkey known in Africa, the last discovery being the sun-tailed monkey, Cercopithecus solatus, found in Gabon in 1984.

Nature
June 7, 2005

Original web page at Nature

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Fastest-evolving genes in humans and chimps revealed

The most comprehensive study to date exploring the genetic divergence of humans and chimpanzees has revealed that the genes most favoured by natural selection are those associated with immunity, tumour suppression, and programmed cell death. These genes show signs of positive natural selection in both branches of the evolutionary tree and are changing more swiftly than would be expected through random mutation alone. Lead scientist Rasmus Nielsen and colleagues at the University of Copenhagen, Denmark, examined the 13,731 chimp genes that have equivalent genes with known functions in humans.

Research in 2003 revealed that genes involved with smell, hearing, digestion, long bone growth, and hairiness are undergoing positive natural selection in chimps and humans. The new study has found that the strongest evidence for selection is related to disease defence and apoptosis – or programmed cell death – which is linked to sperm production. Nielsen, a professor of bioinformatics, believes immune and defence genes are involved in “an evolutionary arms race with pathogens”. “Viruses and other pathogens evolve very fast, and the human immune system is constantly being challenged by the emergence of new pathogenic threats,” he told New Scientist. “The amount of selection imposed on the human population by pathogens – such as the bubonic plague or HIV – is enormous. It is no wonder that the genes involved in defence against such pathogens are evolving very fast.”

Harmit Singh Malik, a researcher at the Fred Hutchinson Cancer Research Center in Seattle, Washington, US, agrees. Both Malik and Nielsen, however, expressed surprise over the findings concerning tumour suppression, which is linked to apoptosis – or programmed cell death – which can reduce the production of healthy, mature sperm. The discovery by Nielsen that genes involved in apoptosis show strong evidence for positive natural selection may be due, in part, to the evolutionary drive for sperm cells to compete.

Cells carrying genes that hinder apoptosis have a greater chance of producing mature sperm cells, so Nielsen believes these genes can become widespread in populations over time. But because primates also use apoptosis to eliminate cancerous cells, positive selection in this case may not be favourable for the mature animal: “The selfish mutations that cause apoptosis avoidance may then also reduce the organism’s ability to fight cancer,” Nielsen explains.

Journal reference: Public Library of Science Biology (vol 3, issue 6)

New Scientist
May 24, 2005

Original web page at New Scientist

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Mystery of Gibraltar monkeys explained

Scientists have used DNA to figure out the origin of Gibraltar’s Barbary macaques, which may have played a small part in winning World War II. The macaques have long been figures of Gibraltar lore. As the story goes, when they are gone, the disputed British colony will return to Spanish rule.

In 1942, a handful of the monkeys remained. Gibraltar was militarily important, and any jolt to morale had to be avoided. Britain’s Prime Minister Winston Churchill sent out a secret edict: Get more monkeys and bring them to the rock. “Nobody knows where they got the macaques — they just suddenly appeared in Gibraltar,” said Robert D. Martin, provost for academic affairs at the Field Museum in Chicago. Martin and colleagues Lara Modolo and Walter Salzburger provided a partial answer in a paper published online this week in the Proceedings of the National Academy of Sciences.

The scientists used DNA comparisons to conclude that the creatures came from two places — Morocco and Algeria, the only regions where Barbary macaques still reside in the wild. Macaques from these two places are genetically distinct. Martin said the mixed origins of the imported macaques helped explain why the roughly 200 macaques now in Gibraltar were relatively healthy despite the inevitable inbreeding. “My expectation was that the macaques in Gibraltar would be a genetic disaster area,” he said. “But when we looked, their genetics was a lot more varied than I expected.” If the legend is true, Spain may have to wait a while before it gets Gibraltar back.

Yahoo
May 24, 2005

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Practice doesn’t make perfect for duelling meerkats.

Vigorous play fighting as a pup does not improve a meerkat’s chances in important adult battles, dispelling the most popular theory to explain youthful brawls. As juveniles, many animals indulge in dangerous and energetically costly battles with litter-mates or other youngsters. Biologists have often assumed the rationale behind this play fighting is to develop the motor skills and coordination necessary for successful adult fights.

For meerkats the stakes are particularly high as only the dominant male-female pair in a colony gets to breed. The others are condemned to mere nest attendant duties. Lynda Sharpe at the University of Stellenbosch, South Africa, studied a population of wild meerkats in the southern Kalahari desert in South Africa from 1996 to 2002. She followed 18 pairs of same-sex litter-mates, recording the number, frequency and outcome of play fights and the individuals’ ultimate status within the group as an adult.

She found that young meerkats who played frequently were no more likely to win play fights, adult fights or become a member of the dominant pair. Furthermore, meerkats showed no sign of improvement with extra play sessions. Sharpe believes that while play fighting may not produce highly trained combatants it could have an important role in brain development.

New Scientist
May 10, 2005

Original web page at New Scientist

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Rare baby aye-aye hand-reared in British zoo

A rare species of lemur, the distinctive-looking and endangered aye-aye, has been bred in captivity and now is being hand-reared in a British zoo, zookeepers said. Kintana, eight weeks old, is only the second aye-aye to be hand-reared in the world, and requires round-the-clock attention from its two keepers. Its birth was hailed by Bristol Zoo Gardens, in the west of England, as an important step in the long-term survival of Madagascar aye-ayes, classified as endangered species and present in just 10 zoos around the world.

Kintana, who weighs 365 grams (12 ounces), is being fed a diet of soy milk, and will eventually be returned to its mother. “In the first few weeks, I was feeding him every two hours through a syringe with a plastic nibble, which meant setting my alarm throughout the night,” said Caroline Brown, one of the zookeepers. “At the moment, he can sit in the palm of my hand, but he is growing every day and can hold his heap and walk about more confidently,” Brown said.

The nocturnal aye-aye, with yellow eyes, big ears, spiky hair and scary fingers, has long been persecuted in its native Madagascar for its unusual looks and the belief that its presence is an ill omen.

For picture of aye-aye activate Original web page at Yahoo.

Yahoo
April 26, 2005

Original web page at Yahoo