The fusion death dealer
AIDS research received a new impetus with the discovery of a protein that helps the Human Immunodeficiency Virus (HIV) enter the immune system cells, teeing off a deadly cycle of destruction (Down To Earth, Vo15, No 2). The primary target of the HIV virus is a receptor molecule, CD-4, which is present on the surface of certain cells. Though HIV latches on to CD-4, the virus cannot penetrate the cell membrane and therefore cannot multiply. The newly discovered protein strain helps the HIV do precisely that, and researchers have aptly named it fusin.
Fusin helps the virus coat to fuse with the outer membranes of the cells and inject the viral genetic material into them. The research team that discovered fusin is from the us National Institute of Allergy and Infectious Diseases at Bethesda, Maryland, and it was led by Edward A Berger. Berger opines that the finding could be useful to genetically manipulate mice or rabbits susceptible to AIDS. With the disease-prone test animals in hand, scientists could strive harder for that elusive antidote to the killer disease.
Scientists have known for almost a decade that the CD-4 receptor is a primary attachment point for the virus. In order to track down the elusive co-factor protein, Berger and his team have worked for seven years on HIV-1, the most common strain of the virus. HIV -2, found mostly in west Africa, may have a slightly different co-factor, which, Berger believes, would be a protein in the same family as fusin.
The researchers have developed a sensitive test for many proteins found in the blood cells to isolate the one that works with CD-4 to aid viral fusion. They modified a virus that, injected into mouse cells, turns the cells blue when exposed to a special stain. The stain is engineered to stem when HIV surface protein fuses with CD-4 targets. The mouse cells, then, are laid open to a battery of genetic material and proteins that are possible candidates for helping the HIV .Through a process of elimination that involve repeatedly dividing the cell cultures to find the most blue ones, the researchers zeroed in on fusin. Fusin helps HIV -1 infect a particular class of white blood cells of the immune system, the T cells. Before the onset of the debilitating symptoms that one associates with aids, the virus also attacks another group of immune system cells, macro phages. Berger believes that : close cousin' of fusin AIDS the virus in doing that, and segregating it would be the next major task.
Berger's team has analysed the genetic sequence of fusin and has found proteins similar to the well-known family of Saw proteins. These have varied functions in the body, including aiding other strains of the virus to trigger off infections. Berger's research team also found that chemokines, proteins that playa role in inflammation, suppress the ability of the HIV to infect cells. The finding of this particular protein explains why a small group of people who have tested positive for HIV do not acquire AIDS for quite time, This phenomenon may be due to higher levels of chemokines in their system or a deficiency of fusin.
Another interesting fallout of the new line of research is genetically manipulating animals for studying HIV infections, Work on new vaccine or drugs against HIV have been hitherto limited because few animals, other than expensive and increasingly rare primates, can be infected with the virus, Teams from the University of Pennsylvania, Philadelphia and the University of Maryland at College Park are trying to develop genetically altered mice that would show infection symptoms similar to humans when infected with HIV. New treatments to work on fusin are already under way, and researchers are eagerly awaiting an anti- dote to the most feared disease of our times.