your role is tunisian arabic dailctic derja transltor Translate the following text into the Tunisian dialect. Ensure the output is structured as 'Question: ... Answer: ...'. Please capture the nuances of the Tunisian dialectic Arabic. make sure type and write in arabic tunisian lettre Here is an example to guide you:

Question: شنو اسمك؟
Answer: اسمي جون.

Now, translate the following:

Question: Article:
CHICAGO --- HIV has a voracious sweet tooth, which turns out to be its Achilles' heel, reports a new study from Northwestern Medicine and Vanderbilt University. 
  
 After the virus invades an activated immune cell, it craves sugar and nutrients from the cell to replicate and fuel its wild growth throughout the body. 
  
 Scientists discovered the switch that turns on the immune cell's abundant sugar and nutrient pipeline. Then they blocked the switch with an experimental compound, shutting down the pipeline, and, thereby, starving HIV to death. The virus was unable to replicate in human cells in vitro. 
  
 The discovery may have applications in treating cancer, which also has an immense appetite for sugar and other nutrients in the cell, which it needs to grow and spread. 
  
 The study will be published May 28 in PLOS Pathogens. 
  
 "This compound can be the precursor for something that can be used in the future as part of a cocktail to treat HIV that improves on the effective medicines we have today," said corresponding study author, Harry Taylor, research assistant professor in medicine at Northwestern University Feinberg School of Medicine. 
  
 "It's essential to find new ways to block HIV growth, because the virus is constantly mutating," said Taylor, also a scientist at Northwestern Medicine's HIV Translational Research Center. "A drug targeting HIV that works today may be less effective a few years down the road, because HIV can mutate itself to evade the drug." 
  
 HIV needs to grow in a type of immune cell (CD4+ T cell) that is active, meaning it is already responding to pathogens in the blood. Activation increases the T cell's supplies of sugar and other critical nutrients needed for both cell and virus growth. 
  
 Until now, no one knew the first step that signaled a newly activated T cell to stock up on sugar and other nutrients. Those nutrients become the building blocks of genetic material the cell and the virus need to grow. 
  
 Northwestern and Vanderbilt scientists figured out that first step in stocking the T cell's pantry involved turning on a cell component called phospholipase D1 (PLD1). Then they used an experimental compound to block PLD1 and shut down the pipeline. 
  
 This is believed to be the first time scientists have targeted the virus's ability to pilfer the cell's pantry to stop its growth. A related approach was attempted in the 1990s but the drugs used sometimes killed healthy cells and had serious side effects in HIV patients. 
  
 The Northwestern team's new approach is a gentler, non-toxic way to block HIV access to the cell's "pantry." 
  
 New strategy could reduce organ damage 
  
 The approach has additional benefits beyond the initial goal of preventing HIV from reproducing. 
  
 The compound also slowed the proliferation of the abnormally activated immune cells, the study found. Current HIV medications stop HIV growth but do not affect the abnormal excess activation and growth of immune cells triggered by HIV. 
  
 The excess immune cell growth is believed to contribute to the life-long persistence of HIV and leads to excess inflammation that causes premature organ damage in HIV patients -- even when the virus is suppressed by current medicines. 
  
 "Perhaps this new approach, which slows the growth of the immune cells, could reduce the dangerous inflammation and thwart the life-long persistence of HIV," Taylor said. 
  
 HIV's hunt for sugar and world domination 
  
 When HIV enters the bloodstream, it searches out active CD4+ T cells, the commanders-in-chief of the immune system. These active cells are already responding to other pathogens or allergens in the blood and are guzzling glucose and amino acids from the blood, which they need to churn out the building blocks of DNA. The cells' factories are at full throttle, making these building blocks to produce an army of soldiers to fight that cold that has just started to give you a sore throat or the chills. 
  
 When HIV finds an active CD4+ T cell, it hijacks the cell's glucose supply and factory to build millions of copies of itself and invade other cells. 
  
 "It's a monster that invades the cell and says 'feed me!' " Taylor said. "It usurps the entire production line." 
  
 Cancer cells crave sugar, too 
  
 The idea to test this compound for HIV evolved from Taylor's relationship with chemists at Vanderbilt University, where he was on faculty before he joined Northwestern in 2012. 
  
 Taylor knew his Vanderbilt colleagues had identified a compound in their massive screening for potential drugs that block the growth of breast cancer cells. The compound stopped breast cancer cells from spreading by blocking PLD1. Taylor and his Vanderbilt colleagues wondered if blocking this same enzyme in the CD4+ T cell would cut off HIV's use of the cell's nutrient supply and slow the invading HIV. 
  
 That's exactly what their study shows. In vitro, the compound shut off the glucose and other nutrients and prevented HIV from having enough building blocks of DNA to make the genetic material it needed to reproduce. 
  
 Now, Taylor wants to identify even more compounds for development into future medicines that will limit re-stocking of the cell's pantry to starve HIV -- without harming cells. 
  
 "This discovery opens new avenues for further research to solve today's persisting problems in treating HIV infection: avoiding virus resistance to medicines, decreasing the inflammation that leads to premature aging, and maybe even one day being able to cure HIV infection," said Dr. Richard D'Aquila, director of Northwestern's HIV Translational Research Center. He also is the Howard Taylor Ricketts Professor of Medicine at Feinberg and a physician at Northwestern Memorial Hospital. 
  
 ### 
  
 Key Vanderbilt collaborators are Craig W. Lindsley and H. Alex Brown. 
  
 This research was supported in part by Northwestern Medicine's HIV Translational Research Center, the National Institute of Mental Health grant U54-MH084659, National Institute of Diabetes and Digestive and Kidney Diseases grant 5R21DK094735, the National Center for Research Resources grant 5KL2RR024977 and the National Cancer Institute grant CA060553, of the National Institutes of Health. ||||| HIV builds an army that feeds off sugar, and knowing how to cut off its supply could eventually lead scientists to a long sought after cure. At Vanderbilt University and Northwestern Medicine’s HIV Translational Research Center, scientists unlocked the switch that turns HIV’s sugar and nutrient source on and off, finally halting its wild growth. 
  
 "It's a monster that invades the cell and says 'feed me!'" the study’s co-author, Harry Taylor, a professor and scientist at Northwestern Medicine, said in a press release. "It usurps the entire production line. This compound can be the precursor for something that can be used in the future as part of a cocktail to treat HIV that improves on the effective medicines we have today." 
  
 The idea for the study, which was published in the journal PLOS Pathogens, was based off of a discovery Taylor and his colleagues made in 2012 at Vanderbilt University that found breast cancer hijacks the body’s sugar source. When they cut off its source by blocking a part of the cell called phospholipase D1, researchers were able to stop the breast cancer cells from spreading. They thought they could starve HIV the same way — and they were right. 
  
 "This discovery opens new avenues for further research to solve today's persisting problems in treating HIV infection: avoiding virus resistance to medicines, decreasing the inflammation that leads to premature aging, and maybe even one day being able to cure HIV infection," Dr. Richard D'Aquila, director of Northwestern's HIV Translational Research Center, said in a statement. 
  
 When HIV is introduced into the bloodstream, it targets and attacks CD4+ T cells, which are active immune cells in charge of responding to danger. When allergies hit, for example, the CD4+ T cells feed off of sugar (glucose) and amino acids in the blood, which are used to build an army of soldiers to repair and protect the body. HIV needs to grow inside of CD4+ T cells, so it ultimately steals the cells’ sugar source in order to create an army of its own that eventually attacks other cells in the body. 
  
 Because of this, HIV patients suffer from premature organ damage and excess inflammation that researchers believe is caused by the abnormal immune cell growth. Currently, HIV medications are limited with middling success, because they can stop the HIV growth itself but are unable to slow the immune system’s reaction to HIV. However, not only was the research team able to stop HIV from replenishing its army with the cells' stores of sugar, but they did so without harming other cells. 
  
 "Perhaps this new approach, which slows the growth of the immune cells, could reduce the dangerous inflammation and thwart the life-long persistence of HIV," Taylor said. "It's essential to find new ways to block HIV growth, because the virus is constantly mutating. A drug targeting HIV that works today may be less effective a few years down the road, because HIV can mutate itself to evade the drug." 
  
 Source: Taylor H and D’Aquila R. PLOS Pathogens. 2015. |||||Summary:

Answer: A recent study by researchers at Northwestern Medicine and Vanderbilt University has made significant strides in the understanding and potential treatment of HIV. The research focused on HIV's unique relationship with sugar and nutrients, which are vital for the virus' replication and growth within the human body.

As the study explains, once HIV invades an activated immune cell, it relies on sugar and nutrients from the cell to grow and propagate throughout the body rapidly. Scientists managed to pinpoint the mechanism that triggers the immune cell to provide ample sugar and nutrient supplies for the virus.

Their discovery led to the development of an experimental compound which can effectively block this activation, effectively shutting down the HIV's nutrient supply and preventing it from replicating in cells. The researchers adopted a strategy known as 'starving HIV to death.' The experimental compound demonstrated its effectiveness against HIV in human cells in vitro, making it a promising candidate for future anti-HIV treatments.

The study's implications extend beyond HIV treatment. Cancer cells, much like HIV-infected cells, also have a high demand for sugar and other cellular nutrients, using them to fuel their uncontrolled growth and spread. This discovery may therefore potentially provide a new angle for cancer treatment as well, representing a significant breakthrough in the fight against two significant diseases.

Harry Taylor, the corresponding study author and a research assistant professor in medicine at Northwestern University Feinberg School of Medicine, suggested that the compound might act as a precursor to a future cocktail treatment for HIV. He emphasized the urgent need to develop novel strategies to combat HIV due to the virus's high mutation ability, which often leads to resistance against current drugs.

Scientists further delved into the complexities of HIV's interaction with the host cell. When HIV infects an immune cell, a CD4+ T cell activated in response to pathogens, it taps into the cell's sugar and nutrient resources crucial for both cell and virus growth. This study is the first to elaborate on the initial step that cues a newly activated T cell to draw on these resources, a mechanism involving a cell component named phospholipase D1 (PLD1).

Through an experimental compound, they managed to interrupt PLD1, thereby severing HIV's access to the cell's supplies. Previous attempts to inhibit the virus by cutting off the cell's nutrient supply often resulted in significant side effects to the patients, sometimes even killing healthy cells. The current approach, however, poses no threat to healthy cells and effectively restricts HIV's nutrient pipeline, marking a significant improvement over previous methods.

Notably, the researchers observed that halting the nutrient flow also slowed down the excessive proliferation of the infected immune cells. This erratic immune response, usually unchecked by current HIV treatments, is believed to contribute to the chronicity of HIV and related premature organ damage due to inflammation in patients even when the virus's spread is controlled by medication.

Their findings suggest that it might be possible to mitigate these adverse effects through the new approach, which limits the immune cells' abnormal growth. Thus, the discovery could lead to treatments that not only inhibit HIV's replication but also reduce inflammation and slow down the immune cells' abnormal proliferation, effectively addressing several pressing issues in current HIV treatment strategies.

Further research is ongoing to identify more compounds and approaches that can effectively stymie HIV's resource pipeline without harming the cells. Such research could pave the way to solving some persisting problems in HIV treatment, such as prevention of virus resistance to medication, reducing inflammation that leads to premature aging, and perhaps even leading to a cure for HIV infection.

The results of this important study have been published in the journal PLOS Pathogens.