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Home » CCR5-DELTA 32

CCR5-DELTA 32

CCR5-DELTA 32

GS 3 – Indigenization of technology and developing new technology; Awareness in the fields of biotechnology.

 

In news: The remarkable research breakthrough that appears to have cured the anonymous “London Patient” of HIV is based on a stem cell transplant involving CCR5-delta 32 homozygous donor cells. This is the same treatment that cured Timothy Ray Brown, known as the “Berlin Patient” when he received two stem cell transplants in 2007 and 2008. In 2009, Brown’s doctor, Berlin-based haematologist Gero Hütter, reported success and a decade on, the American recipient of his treatment remains HIV-free.

 

CCR5-delta 32

Cysteine-cysteine chemokine receptor 5 (CCR5) is found in the cell membranes of many types of mammalian cells, including nerve cells and white blood cells. The role of CCR5 is to allow entry of chemokines into the cell—chemokines are involved in signaling the body’s inflammation response to injuries.

The gene that codes for CCR5 is situated on human chromosome 3. Various mutations of the CCR5 gene are known that result in damage to the expressed receptor. One of the mutant forms of the gene is CCR5-delta32, which results from deletion of a particular sequence of 32 base-pairs. This mutant form of the gene results in a receptor so damaged that it no longer functions. But surprisingly, this does not appear to be harmful.

Moreover, this mutation can be advantageous to those individuals who carry it. The virus HIV normally enters a cell via its CCR5 receptors, especially in the initial stage of a person becoming infected. But in people with receptors crippled by the CCR5-delta32 mutation, entry of HIV by this means is blocked, providing immunity to AIDS for homozygous carriers and greatly slowing progress of the disease in heterozygous carriers.

HIV

HIV is a virus spread through certain body fluids that attacks the body’s immune system, specifically the CD4 cells, often called T cells. Over time, HIV can destroy so many of these cells that the body can’t fight off infections and disease. These special cells help the immune system fight off infections. Untreated, HIV reduces the number of CD4 cells (T cells) in the body. This damage to the immune system makes it harder and harder for the body to fight off infections and some other diseases. Opportunistic infections or cancers take advantage of a very weak immune system and signal that the person has AIDS.                  

 

Treatment so far

No effective cure currently exists for HIV. But with proper medical care, HIV can be controlled. Treatment for HIV is called antiretroviral therapy or ART. If people with HIV take ART as prescribed, their viral load (amount of HIV in their blood) can become undetectable. If it stays undetectable, they can live long, healthy lives and have effectively no risk of transmitting HIV to an HIV-negative partner through sex. Before the introduction of ART in the mid-1990s, people with HIV could progress to AIDS (the last stage of HIV infection) in a few years. Today, someone diagnosed with HIV and treated before the disease is far advanced can live nearly as long as someone who does not have HIV.

Ongoing research on CCR5

On the surface membrane of immune cells is a protein called CCR5, which is, as a post on the Nature Education blog Scitable puts it, “like a door that allows HIV entrance into the cell”. However, about 1% of people of Northern European descent, mainly Swedes, are born  with a mutation known as CCR5-delta 32, which “locks ‘the door’ which prevents HIV from entering into the cell”.

                            Simply put, HIV uses the CCR5 protein to enter immune cells, but it can’t latch on to cells that carry the delta 32 mutation. IciStem, a consortium of European scientists studying stem cell transplants to treat HIV infection, has a database of 22,000 donors with this HIV-resistant mutation.

                             IciStem scientists are tracking 38 HIV-infected people who have received bone-marrow transplants, including six from donors without the delta 32 mutation. The London Patient is 36 on that list; Number 19, the so-called “Düsseldorf Patient”, has been off anti-HIV drugs for four months now, The New York Times reported. Incidentally, CCR5 is the protein that Chinese scientist He Jiankui claimed to have modified with CRISPR/Cas9 gene editing in at least two children in an attempt to make them resistant to HIV.

 

Previous Year Questions

  1. What do you understand by Fixed Dose drug Combinations (FDCs)? Discuss their merits and demerits.(2013)
  2. Scientific research in Indian universities is declining, because a career in science is not as attractive as are business professions, engineering or administration, and the universities are becoming consumer-oriented. Critically comment. (2014)
  3. Can overuse and free availability of antibiotics without Doctor’s prescription, be contributors to the emergence of drug-resistant diseases in India? What are the available mechanisms for monitoring and control? Critically discuss the various issues involved. (2014)
  4. Why is nanotechnology one of the key technologies of the 21st century? Describe the salient features of Indian Government’s Mission on Nano science and Technology and the scope of its application in the development process of the country. (2016)