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diagram of a human immunodeficiency virus

Last week, we gave a general background of human immunodeficiency virus (HIV), the virus that causes AIDS by destroying the immune system. But how is HIV able to disable our immune systems so effectively, anyway? The answer lies in its structure.

HIV, just like any other virus, is made up of a tiny capsule with a small piece of genetic code inside. While most viruses we’re familiar with store their genes on a molecule called DNA, HIV contains two pieces of RNA, which is another type of gene-storing molecule. The HIV capsules also contain an enzyme called transcriptase, which “translates” the RNA into a strand of DNA that our cells can read. Our cells are then tricked into reading this DNA and producing more copies of the virus — which are then released from the host cell, at which point they are free to infect other cells. In this manner, an HIV infection slowly grows.

HIV targets our immune systems, the very mechanism that evolved to keep us safe from pathogens.

When a virus is introduced into a host’s body, immune cells pick it up and carry it to the lymphoid organs — which are a sort of meeting place for other types of immune cells, including CD4+ T helper cells (also called helper T cells). Helper T cells enlist the help of other immune cells, called killer T cells, which destroy cells infected with viruses. Helper T cells also activate the production of antibodies, molecules that are specialized to attach to a specific pathogen so that it can be destroyed. Normally, this is where the virus meets its end. Unfortunately, HIV is different from run-of-the-mill viruses in that it is specialized to invade helper T cells. Now, instead of coordinating an attack against HIV, the helper T cells have been hijacked — converted into factories for the production of yet more HIV. Continue reading →

This scanning electron micrograph shows HIV particles (colored yellow) infecting a human T cell. Image: National Institute of Allergy and Infectious Diseases, National Institutes of Health

In 2006, an HIV-positive man was diagnosed with leukemia. First he received chemotherapy, and when the cancer returned his doctor recommended a stem-cell transplant with tissues obtained from a bone-marrow donor. After finding an unusually high number of compatible donors, his doctor, Gero Hütter, had a simple idea that would change the course of HIV research. Dr. Hütter knew of a rare genetic mutation that confers immunity to many strains of HIV, including the strain that infected his cancer patient. And new blood cells, including immune cells, are manufactured by bone marrow. What if he could find a bone-marrow donor with this mutation? What effect would it have on the HIV infection?

Five years after his cancer diagnosis, the man, known as the Berlin patient and recently identified as Timothy Ray Brown, is in remission from cancer … and the most sensitive tests have been unable to detect HIV anywhere in his body, despite the discontinuation of antiretroviral drugs. Scientists are a cautious lot, careful not to make grand statements without qualifying them with words like “seem” and “suggest.” But more and more, researchers are starting to say that Brown could be the first case in which a cure for HIV was attained.

Human immunodeficiency virus, or HIV, has been the focus of intense research since the 1980s, when it was identified as the causative agent of AIDS. Many anti-HIV drugs have been developed since then, though worldwide, less than a third of people who need the drugs have access to them. Those with access, however, have significantly improved health outcomes and longer life expectancy. Continue reading →

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