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Scientists Spot New Twist in HIV Infection
 THURSDAY, Sept. 4 (HealthDay News) -- The virus that causes AIDS infects one form of immune T-cell by rearranging its inner skeleton, allowing it access to the cell, scientists have discovered.
The finding helps explain how HIV maintains pockets of dormant virus in these so-called "resting" T-cells, even when the virus is under attack by antiretroviral drugs. It also points to potential new targets for drug development, experts say.
"Whenever you identify a necessary step -- a step which is absolutely required for infection of naive T-cells -- of course then you have a new focus point, one that you can examine to see if there are options for new therapies. Certainly with HIV treatment, we need that," said study co-author Jon Marsh, a researcher in the Laboratory of Cellular and Molecular Regulation at the U.S. National Institute of Mental Health.
Viruses are such primitive life forms that they must gain access to other organisms' genetic material, located deep in the nucleus of the cell, before they can replicate. Scientists have long known that HIV latches onto certain receptors on the surface of its main target -- the immune system's T-cells -- to gain entry into the cell.
Early in the disease process, HIV typically attacks "activated" T-cells -- so named because they are already primed against a particular pathogen. But so-called "naive" T-cells also move throughout the bloodstream. These cells are often resting -- they haven't yet been activated to fight a particular threat.
When HIV seeks entry to the activated T-cell, it does so by latching onto a surface receptor called CCR5. But in more than 50 percent of patients, the virus begins to attack resting T-cells, too, via a receptor called CXCR4.
"We know that HIV prefers to infect activated T-cells -- it's more difficult for HIV to infect resting T-cells," noted Rowena Johnston, vice president of research at the Foundation for AIDS Research (amfAR) in New York City. "So, the question for me and a lot of people has been: Why does the virus do it? What possible advantage could there be?"
In their new research, Marsh and study co-author Yuntao Wu, of George Mason University, believe they may have answered that question. They published the findings in the Sept. 5 issue of Cell.
According to the researchers, HIV binds with the CXCR4 receptor on resting T-cells, and that activates a protein called cofilin. Cofilin effectively rearranges the tiny filaments that make up the T-cells protective inner skeleton. One this is done, HIV is able to sneak past this barrier and into the cell's nucleus.
"So now HIV has a means of making these normally [highly] resistant cells susceptible to infection," Marsh said.
For HIV, there's a decided plus to entering resting versus activated T-cells, because resting cells provide a much safer hiding place, Johnston noted. "If it can get into the resting T-cell, it can just sit in that-cell forever," she explained. "This induces latent infection."
HIV is known to hide out in a number of cell types in the body, making a cure for AIDS elusive. "But if we are aiming to cure infection, we need to understand all of the ways in which latent infection can be established," Johnston said.
HIV's entry into resting T-cells also marks more advanced disease, the experts said. "The emergence of CXCR4 [type virus] usually is late in the disease, and it's usually associated with a relatively severe decline in CD4 T-cells. So, it's not a good sign," Marsh said.
Will this discovery inevitably lead to new, effective AIDS drugs? That remains uncertain, Marsh said.
"The thing about a virus is that it exploits normal processes in a cell," he explained. "So, the clinical aspect always has to look for ways in which you can disturb only the virological component, or most of the virological component, and not hinder those things that are most absolute and necessary for life."
Johnston agreed it may be years, if ever, before this discovery leads to effective therapies. Right now, she said, "this is very much in the arena of just understanding how HIV does what it does."
More information
Find out more on the fight against HIV/AIDS at amfAR  .
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'Bonding Gene' Could Help Men Stay Married
MONDAY, Sept. 1 (HealthDay News) -- Whether a man has one type of gene versus another could help decide whether he's good "husband material," a new study suggests.
A study of Swedish twin brothers found that differences in a gene modulating the hormone vasopressin were strongly tied to how well each man fared in marriage.
"Our main finding was an association between a variant of the vasopressin receptor 1a gene and how strong bonds men reported they had to their partners," said lead researcher Hasse Walum, of the department of medical epidemiology and biostatistics at the Karolinska Institute in Stockholm. "Men carrying this variant scored on average lower on a scale measuring the strength of the bond compared to men not carrying this variant."
Women married to men carrying the "poorer bonding" form of the gene also reported "lower scores on levels of marital quality than women married to men not carrying this variant," Walum noted.
His team published its findings in this week's issue of the Proceedings of the National Academies of Science.
Walum's team first got interested in the role of vasopressin and bonding among males when studying a rodent, the vole. "Studies in voles have shown that the hormone vasopressin is released in the brain of males during mating," Walum explained.
Vasopressin activates the brain's reward system, and "you could say that mating-induced vasopressin release motivates male voles to interact with females they have mated with," Walum said. "This is not a sexual motivation, but rather a sort of prolonged social motivation." In other words, the more vasopressin in the brain, the more male voles want to stick around and mingle with the female after copulation is through. This effect "is more pronounced in the monogamous voles," Walum noted.
But voles and humans are very different species, so would the same effect hold true for men?
To find out, the Swedish team zeroed in the vasopressin 1a gene, which is shared by both species. Variations in this gene strongly influence vasopressin activity in the male vole, so Walum wondered if it might do the same for men.
To find out, his team looked for variants of the vasopressin 1a gene among 552 pairs of male twins enrolled in Sweden's ongoing Twin and Offspring Study. All of the men were currently in a relationship that had lasted at least five years, although about 18 percent of the men remained unmarried. The men were subjected to psychological tests assessing their ability to bond and commit, and the researchers also interviewed the men's spouses when possible.
They found that men with a certain variant, known as an allele, of the vasopressin 1a gene, called 334, tended to score especially low on a standard psychological test called the Partner Bonding Scale. They were also less likely to be married than men carrying another form of the gene. And carrying two copies of the 334 allele doubled the odds that the men had undergone some sort of marital crisis (for example, the threat of divorce) over the past year.
All of these findings "make sense," said Dr. John Lucas, a clinical associate professor of psychiatry at Weill Cornell Medical College in New York City. He said it's well known that genes help drive much of human behavior, including mate bonding.
But the vasopressin 1a gene is likely not the only factor influencing a man's ability to form true and lasting bonds, he added.
"It's unlikely to be a single gene [at work] -- it's likely to be multiple genes that are expressed incompletely and interact with the environment," said Lucas, who is also a psychiatrist at New York Presbyterian Hospital/Weill Cornell Medical Center. He pointed out that what psychologists call "temperament" -- the individual palette of emotions and behaviors that even babies display -- is probably "hard-wired" by our genetics. "But temperament, through training and experience, becomes personality," Lucas said. "And personality is a complicated situation, of course, and it involves the ability to commit."
So, it's too early for men to blame their inability to commit on a single gene, although Lucas guesses it's an excuse that's "certainly going to be used."
For his part, Walum agreed that men and their spouses shouldn't read too much into the finding.
"Taken together, the effect of the gene variant that we have studied on human pair-bonding behavior is rather small, and it can not, with any real accuracy, be used to predict how someone will behave in a future relationship," he said.
Walum also noted that the finding would probably not be applicable to women, since vasopressin appears to be tied to social bonding in males, but not females.
In a related study, also in the same issue of the journal, researchers at the Pacific Health Research Institute in Honolulu said they've identified a gene strongly linked to extended health and life span in humans. The FOXO3A gene, involved in insulin signaling, is just the second gene ever found that is closely tied to longevity, the researchers said. In their study of Japanese-American men, those who lived to an average age of 98 had a specific variant of FOXO3A compared to men who died at younger ages, the team said.
More information
There's more on genes and behavior at Stanford University .
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Extremely Preemie Babies Prone to Behavior Woes Later On
 TUESDAY, Sept. 2 (HealthDay News) -- A study looking at children born extremely prematurely (at or before 25 weeks of gestation) finds they are at significantly higher risk for behavior problems by age 6, with boys particularly vulnerable.
"Attention problems and social problems with peers have been reported previously" in children born prematurely, noted study lead author Dieter Wolke, professor of developmental psychology and individual differences at the University of Warwick in the United Kingdom.
But the study, which compared parent and teacher reports of behavior problems at age 6 in 200 children born preterm against 148 children who were born full-term, is more comprehensive, he said, and draws from more than one center. "Most previous studies have used parent reports, very few teacher reports," Wolke said, while his study used both. "Parent reports can be biased," he noted.
The new findings were published in the September issue of the journal Pediatrics.
In the study, teachers and parents were asked about emotional problems, conduct, hyperactivity, peer problems, social behavior and adaptability to school.
Overall, 19.4 percent of the extremely preterm children had behavior problems, but just 3.4 percent of the control children did. "We found that already in 6-year-olds, the extremely preterm child had four times more often emotional problems (anxiety, depression) than controls," Wolke said. "This has not been reported for larger preterm [born after 25 weeks but not full term] children."
Boys were twice as likely as girls to suffer behavioral problems, the researchers found. When they assessed children's cognitive functioning, it explained the hyperactivity and conduct problems, but problems such as poor attention, poor peer relations and emotional problems couldn't be explained by cognitive function, Wolke said.
So what's at the root of the difficulties? It's not known for sure, Wolke said. But he suspects they are due to "altered brain development from white to grey matter that takes place between 24 to 27 weeks' gestation."
The study is a landmark one, noted Dr. K.J.S. Anand, an attending physician at Arkansas Children's Hospital and a professor at the University of Arkansas for Medical Sciences, Little Rock. He has also done much research on the topic.
With his colleagues, Anand has proposed a possible mechanism, saying the problems may be the result of the maternal separation experienced by these extremely premature infants, impacting the developing brain.
Because some children were lost to follow-up, Anand said, "it is likely that their results may even underestimate the true prevalence of these problems in society."
While Wolke said the problems are child-driven, a result of brain development, and that parents as such can't do much, Anand suggested that greater contact between parents and babies during the first days after delivery may help.
More information
To learn more about preterm birth, visit the March of Dimes .
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Ob/Gyn Group Urges Routine HIV Tests for All Women
FRIDAY, Aug. 1 (HealthDay News) -- Minority women are at higher risk for HIV/AIDS, and doctors need to make a special effort to encourage them to be tested for HIV.
That's the new recommendation released Thursday by the American College of Obstetricians and Gynecologists (ACOG).
"Rates of infection among African Americans -- and also among Hispanics -- are much higher than among white women. Sixty-four percent of women with HIV are black, even though blacks only make up about 13 percent of the U.S. population," Dr. Heather Watts, a liaison member to ACOG's Committee on Health Care for Underserved Women, said in an organization news release.
In 2004, HIV infection was the leading cause of death for black women ages 25 to 34. A combination of testing, education, and brief behavioral interventions can help reduce HIV infection rates among minority women, according to the ACOG committee.
"Education plays an important role. Because HIV is more prevalent in their communities, women of color need to know they are more likely to be exposed to HIV," Watts said. "All women should understand how to protect themselves, such as limiting their number of partners and using condoms consistently."
Research has shown that behavioral interventions can increase rates of condom use, reduce risk-taking behaviors, and decrease the spread of sexually transmitted diseases.
"Physicians can explain to their patients that HIV screening is recommended for all adults now and that there are numerous benefits to being tested. We need to continue to destigmatize HIV screening and make it a part of routine care," Watts said.
More information
The U.S. Centers for Disease Control and Prevention has more about women and HIV.
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