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Exercise ‘to Cut Cancer Death Risk’

You can cut your cancer death risk with just 30 minutes of walking daily, for a new study has revealed that physically fit people are less likely to die from the disease.

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Researchers at Karolinska Institute in Sweden have found that people who do at least half-an-hour of exercise everyday have a 34 per cent lower chance of being killed by cancer than those who do not.

“The study shows, for the first time, the effect that very simple and basic daily exercise such as walking or cycling has in reducing cancer death risk in middle-aged and elderly men,” lead researcher Prof Alicja Wolk said.

They monitored the health and exercise levels of over 40,000 men, aged between 45 and 79, for seven years to reach the conclusion, the British Journal of Cancer has reported.

During that time, 3,714 of the participants developed cancer and 1,153 died from their disease. The findings showed that exercise had a significant influence on cancer survival and a smaller impact on incidence.

In fact, men who walked or cycled at least 30 minutes a day were 34 per cent less likely to die from cancer than men who exercised less or not at all. The same activities led to only a five per cent reduction in cancer rates, a result which could be due to chance.

However, a more intensive programme of walking and cycling for between an hour and an hour-and-a-half a day was associated with a 16 per cent lower cancer incidence, the study found.

“This study gives us a clear indication that men who exercise are less likely to die from cancer,” The Daily Telegraph quoted Dr Lesley Walker of Cancer Research UK, which publishes the journal, as saying.

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Sources: The Times Of India

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Ailmemts & Remedies

Attention Deficit Hyperactivity Disorder (ADHD)

Definition:

Attention Deficit Hyperactivity Disorder, ADHD, is one of the most common mental disorders that develop in children. Children with ADHD have impaired functioning in multiple settings, including home, school, and in relationships with peers. If untreated, the disorder can have long-term adverse effects into adolescence and adulthood.

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It is a neurobehavioral developmental disorder affecting about 3-5% of the world’s population under the age of 19. It typically presents itself during childhood, and is characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility. ADHD is currently considered to be a persistent and chronic condition for which no medical cure is available, although medication can be prescribed. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults. About 60% of children diagnosed with ADHD retain the condition as adults. It appears to be highly heritable, although one-fifth of all cases are estimated to be caused from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling.

The scientific consensus in the field, and the consensus of the national health institutes of the world, is that ADHD is a disorder which impairs functioning, and that many adverse life outcomes are associated with ADHD. It has been frequently said by a minority of news sources, social critics, certain religions, and individual medical professionals, to be a controversial disorder. These criticisms fall outside of majority or minority viewpoint and question its causes, its treatment, and even the existence of ADHD.

Classification:
ADHD is a developmental disorder, in that, in the diagnosed population, certain traits such as impulse control significantly lag in development when compared to the general population. Using magnetic resonance imaging, this developmental lag has been estimated to range between 3 years, to 5 years in the prefrontal cortex of those with ADHD patients in comparison to their peers; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioral or neurodevelopmental disorders.
Three forms of ADHD are thought to exist, ADHD-PI or ADHD Primarily Inattentive (previously known as ADD or Attention Deficit Disorder), ADHD-PH/I or ADHD Primarily Hyperactive/Impulsive, and ADHD-C or combined type. The majority of studies have looked at ADHD-C, with much less work done on ADHD-PI. To determine or rule out ADHD information from several key sources is required.


Symptoms:

The most common symptoms of ADHD are distractibility, difficulty with concentration and focus, short term memory loss, procrastination, problems organizing ideas and belongings, tardiness, impulsivity, and weak planning and execution. Not all people with ADHD have all the symptoms. The Diagnostic and Statistical Manual of Mental Disorders categorises the symptoms of ADHD into two clusters: Inattention symptoms and Hyperactivity/Impulsivity symptoms. Most ordinary people exhibit some of these behaviors but not to the point where they seriously interfere with the person’s work, relationships, or studies or cause anxiety or depression. Children do not often have to deal with deadlines, organization issues, and long term planning so these types of symptoms often become evident only during adolescence or adulthood when life demands become greater.

Symptoms of ADHD will appear over the course of many months, and include:

* Impulsiveness: a child who acts quickly without thinking first
* Hyperactivity: a child who can’t sit still, walks, runs, or climbs around when others are seated, talks when others are talking.
* Inattention: a child who daydreams or seems to be in another world, is sidetracked by what is going on around him or her.

Causes:-
According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there are some effective treatments, but no true cure. Evidence suggests that hyperactivity has a strong heritable component, and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology. Candidate genes include dopamine transporter (DAT), dopamine receptor D4 (DRD4), dopamine beta-hydroxylase (DBH), monoamine oxidase A (MAOA), catecholamine-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-HT1B). Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters. Suspect genes include the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI).

Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17. If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a “genetic disease” and is better viewed as a complex interaction among genetic and environmental factors. As the authors of a review of the question have noted, “Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified.”

Studies show that there is a familial transmission of the disorder which does not occur through adoptive relationships.  Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population.[8] While the majority of ADHD is believed to be genetic in nature,[8] roughly one-fifth of all ADHD cases are thought to be acquired after conception due to brain injury caused by either toxins or physical trauma prenatally or postnatally.

Additionally, SPECT scans found people with ADHD to have reduced blood circulation, and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. Medications focused on treating A.D.H.D.(such as methylphenidate) work because they force blood to flow in certain areas of the brain, those that control and regulate concentration, which usually don’t receive a normal or sufficient amount blood flow or circulation in the brains of A.D.H.D. en companying individuals. A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain’s ability to produce dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to “childhood learning problems” in healthy subjects as well.

Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are the molecular abnormality of ADHD or a secondary consequence of a problem elsewhere. Researchers have described a form of ADHD in which the abnormality appears to be sensory overstimulation resulting from a disorder of ion channels in the peripheral nervous system.

An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children. The image on the left illustrates glucose metabolism in the brain of a ‘normal’ adult while doing an assigned auditory attention task; the image on the right illustrates the areas of activity in the brain of an adult who had been diagnosed with ADHD as a child when given that same task; these are not pictures of individual brains, which would contain substantial overlap, these are images constructed to illustrate group-level differences. Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex.[24] A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADHD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADHD patients (relative to the controls). Most notably, lower metabolic activity in one specific region of the left anterior frontal lobe was significantly inversely correlated with symptom severity.[25] These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.[citation needed]

The estimated contribution of non genetic factors to the contribution of all cases of ADHD is 20 percent.[26] The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure. Lead concentration below the Center for Disease Control’s action level account for slightly more cases of ADHD than tobacco smoke (290 000 versus 270 000, in the USA, ages 4 to 15). Complications during pregnancy and birth—including premature birth—might also play a role. It has been observed that women who smoke while pregnant are more likely to have children with ADHD. This could be related to the fact that nicotine is known to cause hypoxia (lack of oxygen) in utero, but it could also be that ADHD women have more probabilities to smoke both in general and during pregnancy, being more likely to have children with ADHD due to genetic factors.

Head injuries can cause a person to present ADHD-like symptoms, possibly because of damage done to the patient’s frontal lobes. Because these types of symptoms can be attributable to brain damage, one earlier designation for ADHD was “Minimal Brain Damage”.

There is no compelling evidence that social factors alone can create ADHD. Many researchers believe that attachments and relationships with caregivers and other features of a child’s environment have profound effects on attentional and self-regulatory capacities. It is noteworthy that a study of foster children found that an inordinate number of them had symptoms closely resembling ADHD. An editorial in a special edition of Clinical Psychology in 2004 stated that “our impression from spending time with young people, their families and indeed colleagues from other disciplines is that a medical diagnosis and medication is not enough. In our clinical experience, without exception, we are finding that the same conduct typically labelled ADHD is shown by children in the context of violence and abuse, impaired parental attachments and other experiences of emotional trauma.” Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

It is believed that there are several different causes of ADHD. Roughly 80 percent of ADHD is considered genetic in nature and the estimated contribution of non genetic factors to the contribution of all cases of ADHD is believed to be 20 percent.. Environmental agents also cause ADHD. These agents, such as alcohol, tobacco, and lead, are believed to stress babies prenatally and cause ADHD. Studies have found that malnutrition is also correlated with attention deficits. Diet seems to cause ADHD symptoms or make them worse. Many studies point to synthetic preservatives and artificial coloring agents aggravating ADD & ADHD symptoms in those affected. Older studies were inconclusive quite possibly due to inadequate clinical methods of measuring offending behavior. Parental reports were more accurate indicators of the presence of additives than clinical tests. Several major studies show academic performance increased and disciplinary problems decreased in large non-ADD student populations when artificial ingredients, including artificial colors were eliminated from school food programs.. Professor John Warner stated, “significant changes in children’s hyperactive behaviour could be produced by the removal of artificial colourings and sodium benzoate from their diet.” and “you could halve the number of kids suffering the worst behavioural problems by cutting out additives”.

In 1982, the NIH had determined, based on research available at that time, that roughly 5% of children with ADHD could be helped significantly by removing additives from their diet. The vast majority of these children were believed to have food allergies. More recent studies have shown that approximately 60-70% of children with and without allergies improve when additives are removed from their diet,   that up to almost 90% of them react when an appropriate amount of additive is used as a challenge in double blind tests,and that food additives may elicit hyperactive behavior and/or irritability in normal children as well.

Diagnosis:
If ADHD is suspected, the diagnosis should be made by a professional with training in ADHD. After ruling out other possible reasons for the child’s behavior, the specialist checks the child’s school and medical records and talks to teachers and parents who have filled out a behavior rating scale for the child. A diagnosis is made only after all this information has been considered.

Many of the symptoms of ADHD occur from time to time in everyone. In those with ADHD the frequency of these symptoms occurs frequently and impairs regular life functioning typically at school or at work. Not only will they perform poorly in task oriented settings but they will also have difficulty with social functioning with their peers. No objective physical test exists to diagnose ADHD in a patient. As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these critera are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

The terminology of ADD expired with the revision of the most current version of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

Treatment:
Effective treatments for ADHD are available, and include behavioral therapy and medications.
Singularly, stimulant medication is the most efficient and cost effective method of treating ADHD. Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. Behavioral Parent Training, behavior therapy aimed at parents to help them understand ADHD, has also shown short term benefits. Omega-3 fatty acids, phosphatidylserine, zinc and magnesium may have benefits with regard to ADHD symptoms.

Comorbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming. Psychosocial therapy is useful in treating some comorbid conditions.

ADHD Medications:

Another part of the treatment program often involves the prescribed use of certain medications. Parents sometimes worry about their children having to rely on medication. But it’s more important to realize that these can help the ADHD child function at his best, and will consequently help him avoid even greater problems.

Parents should expect to receive detailed information about any prescribed medication from their health professional, including the possible side-effects. This information should then be shared with everyone entrusted with the child’s care. Let’s now look at the most common of ADHD medication.

Methylphenidate

The most commonly prescribed ADHD medication is Methylphenidate. This medication is in fact a stimulant, which interestingly in ADHD children often has the reverse effect of calming them down.

Methylphenidate, also known as Ritalin, is commonly taken in pill form. It takes effect quickly, and lasts three to four hours. The child’s prescribed dosage needs to be administered by an informed adult, two or three times a day, depending on the child’s age – usually in the morning before school, and at lunchtime. Methylphenidate is now also available in a single dose, long acting forms. Dextroamphetamine is another medication used to treat ADHD.

Before medication therapy begins, the diagnosis should be well established, and individualized behaviour and educations plans should be in place. In the absence of these other forms of treatment, drug therapy alone is ineffective.

What about “drug holidays”?

In the past, children being treated for ADHD were sometimes given an extended break from taking medication – usually during the summer months when not in school – to minimize potential side effects. But today, most physicians suggest that current ADHD medication therapy can be safely followed year-round, and can continue to be very helpful outside of school as well. The benefits offered by modern ADHD medications as part of a greater treatment plan, usually outweigh the minimized potential for adverse side effects.

What about alternative treatments?

Alternative treatments for the child’s ADHD may be suggested to you, but it’s important to realize there is no significant scientific evidence that any are effective. Some of these controversial treatments include: biofeedback, mega-vitamin and mineral supplements, anti-motion sickness medication, and optometric exercises. Again, none of these approaches have ever been scientifically proven to have any significant effect on ADHD, so they should probably not be relied on.

The need for on-going monitoring

Whatever treatment strategies are undertaken, the child’s condition needs to be regularly monitored by a health professional. It is especially important to check for side-effects; confirm the on-going effectiveness of the program; and if necessary, make adjustments to the treatment plan.

Prognosis:
The diagnosis of ADHD implies an impairment in life functioning. Many adverse life outcomes are associated with ADHD.

During the elementary years, an ADHD student will have more difficulties with work completion, productivity, planning, remembering things needed for school, and meeting deadlines. Oppositional and socially aggressive behavior is seen in 40-70% of children at this age. Even ADHD kids with average to above average intelligence show “chronic and severe under achievement”. Fully 46% of those with ADHD have been suspended and 11% expelled. 37% of those with ADHD do not get a high school diploma even though many of them will receive special education services. The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool.Only 5% of those with ADHD will get a college degree compared to 27% of the general population. (US Census, 2003)

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://en.wikipedia.org/wiki/Attention-deficit_hyperactivity_disorder
http://www.lipsychiatric.com/common-disorders.asp#adhd
http://www.drpaul.com/behaviour/adhdmedi.html

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News on Health & Science

Piercing Can Cause Dental Hazards

Body piercing, especially to the lips and tongue, can cause serious dental complications, according to research conducted by the University of Tel Aviv.

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In the study of 400 consecutive patients, who were aged 20 years on average, every fourth person with a piercing in the tongue or lips revealed symptoms such as gum bleeding.

Some 13.9 per cent had broken teeth or other dental complications, the study found.

Dental professionals were warned of the increasing number of patients with oral piercing and to provide appropriate guidance to patients regarding the health risks.

Sources:The Times Of India

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Advancing Towards Baby Making

DNA fingerprinting will revolutionise the practice of IVF and eliminate multiple pregnancies.

Given a choice, Gita Kapoor, a 37-year-old banker in Bangalore, would have preferred just one child. She and her software engineer husband knew that with their busy work schedules raising even one child wouldn’t be an easy job. Two years ago, they opted for in vitro fertilisation (IVF) at a fertility clinic in their city. Today the Kapoors are proud parents of a pair of chubby twins — a boy and a girl.

It isn’t that the Kapoors are not happy to have more than one child. But they have two children not by choice but because of an inherent shortcoming in the assisted reproduction technique they opted for.

“So far there is no technique available to choose a single, viable embryo for implantation,” says Dr Trichnopoly Chelvaraj Anand Kumar, a veteran andrologist in Bangalore.

As a result, fertility doctors normally implant more than one embryo to increase the chances of pregnancy. “With a single embryo, the success rate of IVF is about 30 to 35 per cent. It goes up to 45 per cent with two embryos,” says Dr Indira Hinduja, who is the first Indian doctor to have produced a test tube baby in India in the 1980s.

There are a number of problems associated with multiple pregnancies. Often, babies born in a multiple birth are premature, have low birth weight and are prone to infections. Also, their mortality rate is slightly on the higher side, notes Dr Hinduja.

But thanks to a team of medical researchers in Australia and Greece, doctors may soon be able to find a way of successfully employing genetic screening to identify embryos that can lead to healthy babies.

In a paper reported in the latest issue of the journal Human Reproduction, the researchers say that DNA fingerprinting, a technique more commonly used in forensic applications and in resolving parenthood controversies, can be a useful tool in fertility clinics. The technique can help pinpoint a handful of genes that can help spot a better embryo that would lead to a successful pregnancy, says Gayle Jones, a researcher at Monash Immunology and Stem Cell Laboratories, Monash University, Australia.

When a couple attends a fertility clinic for IVF, eggs from the woman are fertilised with sperm from the man and the fertilised eggs are allowed to develop in the laboratory until they reach what doctors call the blastocyst phase, or the early stages of embryo formation. This normally takes about five days.

One of the difficult decisions, even for a better-trained fertility expert, is to decide which fertilised egg is to be chosen. With little help from technology to distinguish a viable blastocyst from a non-viable one, they often resort to implanting more than one to increase the chances. This often leads to multiple pregnancy.

But this need not be the case anymore, say researchers at Monash University and the Centre for Human Reproduction at Genesis Athens Hospital in Greece.

For their study, the scientists removed a few cells each from the outermost layer of the resulting blastocysts of 48 women who attended the clinic for IVF treatment.

Of the 48 women, 25 became pregnant, leading to the delivery of 37 babies. Once the babies were born, blood from the umbilical cords or swabs of cheek cells was collected. Subsequently, the scientists used DNA fingerprinting to see which genes were common to the material collected after delivery as well as the blastocyst biopsy.

“By analysing these genes, we have been able to identify those that are key to the processes involved in embryo implantation,” Jones told KnowHow.

Though it is too early, she thinks that they would be in a position to refine the gene set further to a smaller number of genes that are more highly predictive of a viable blastocyst. “The ability to select a single, most viable embryo from a cohort available for transfer will revolutionise the practice of IVF, not only improving pregnancy rates but also eliminating multiple pregnancies and the attendant complications,” Jones said.

The Monash University researchers hope that the technique would be available for clinical use within a couple of years if they achieve further success.

IVF being the most common and cheapest of all assisted reproductive methods in use, such improvements in its success rate will be a boon to a large number of infertile couples, says Dr Kumar.

Sources:The Telegraph (Kolkata, India)

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News on Health & Science

Games the Aids Virus Plays

The AIDS virus has changed its path to target cells in Westerners but not in Indians because of a high level of pre-existing infections.

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The human immunodeficiency virus (HIV), discovered 25 years ago, has emerged as the most intensely investigated virus in all of human history. Despite this, it remains a biological mystery. One unsolved riddle had been a change in the molecular address —– the gateway –– that HIV uses to enter its target cells in the human body. The change is widely seen in the West, but almost never in India.

Now a team of biologists in New Delhi and Chandigarh has come up with a possible explanation for why this switch in the gateway isn’t observed in Indians: high levels of background infections. Their study has provided fresh insights into the evolutionary tricks that HIV has acquired to continue multiplying in an infected person, while constantly evading destruction.

“This is primarily an exploration of the basic biology of HIV, but it could also have ramifications for future strategies to treat infected people,” said Shahid Jameel, the head of Virology at the International Centre for Genetic Engineering and Biotechnology, New Delhi, who led the study. The findings have just been published in the Journal of Clinical Virology.

The virus uses two key protein molecules to enter its target human T-cells — the main CD4 receptor protein, and a receptor called CCR5 (or R5). They are found on the surface of some T-cells and serve as molecular gateways required for the virus to slip inside the cells. The infection starts with HIV being capable of using the R5 protein.

Previous studies in Western populations, most of them conducted in the United States, have shown that as the infection progresses over time in an infected person, the virus multiplies and evolves and loses its ability to exploit R5, but begins to use another surface protein called CXCR4, or X4, to invade T-cells.

About half of HIV in late infection among Western populations are viruses that use X4. The switch appears to coincide with the advance of the infection to the full-blown AIDS, the onset of life-threatening infections that mark the end stage of the illness.

But virtually all viruses from Indians and some African populations display no such gateway switch from R5 to X4.

“This switch takes places to maximise the infectivity of HIV,” said Jameel. After the initial infection, HIV has to multiply and infect more T-cells. But not all T-cells have R5 on their surface.

Infections can activate T-cells, triggering the appearance of R5 on them. Most people in India are constantly exposed to a high burden of infections –— viral, bacterial, parasitic –— and thus have a high load of T-cells with the R5 protein to fight off such infections.

“Since there are plenty of cells with the R5 protein in Indian patients, there is no evolutionary pressure on the virus to make the switch towards X4,” Jameel said. His team at the ICGEB and a collaborator, Ajay Wanchu of the Postgraduate Institute of Medical Education and Research, Chandigarh, examined the T-cells from 40 HIV positive people who had not started any drug therapy.

The researchers also found that T-cells in infected Indians show less of the R5 protein than in infected Westerners. Viruses that use R5 tend to reduce levels of R5 protein in infected people, while viruses that use X4 tend to reduce the X4 protein.

“This could be a survival strategy of the virus,” Jameel said.

It might be an adaptation to prevent infection of the same cell with more than one virus which, he said, can be detrimental to the virus.

Infection by multiple viruses can trigger a death response which no longer supports viral replication,” he explained.

But some researchers believe that results from studies that rely on T-cells from the bloodstream need to be viewed with caution because the infection is actually in the lymphatic system –— such as the lymph nodes. The vast majority of the T-cells are in lymphatic tissues, and not in blood, said Udaykumar Ranga, a virologist at the Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore.

“The T-cells from blood are not representative of the T-cells in the lymphatic system,” Ranga said. However, most similar studies have used T-cells from blood because it is not ethically possible to get T-cells from the lymphatic system, which would require conducting a biopsy on an infected person’s lymph nodes. “This is a technical limitation of such studies,” Ranga said.

Studies to investigate the switch from the R5 to the X4 receptor are primarily basic research, aimed at exploring how HIV interacts with its human host. But the absence of this switch among Indian patients may have clinical ramifications for future ways of treating HIV infected patients, said Jameel.

A drug that specifically deactivates or blocks the R5 receptor might turn out to be useful in populations where the switch from R5 to X4 does not take place, such as India. “Such a drug could be effectively used in our patients since HIV strains in our population infect exclusively through R5 and not through X4,” Jameel said.

But with HIV, no one is willing to place bets. “It would be interesting to see if the virus switches to X4 or not in patients treated with such a drug,” he said.

Sources:The Telegraph (Kolkata, India)

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