Researchers may have figured out why the body is so slow in producing effective antibodies against HIV. According to study details published in the July 2009 online issue of PLoS Medicine, HIV cripples the production of antibody-producing B cells within just 17 days after infection.

Antibodies are small proteins that kill foreign organisms or tag them for removal by immune system cells. They are produced by B cells and are specific to individual infections. In HIV, the development of antibodies against the strain of virus that enters the body is quite sluggish—sometimes taking months to be produced in sufficient quantities. By contrast, many other viral and bacterial infections trigger robust antibody production within days of infection. Thus far, however, no one has been able to explain and prove why the antibody response in HIV is so slow.

To answer that question, Marc Levesque, MD, PhD, from Duke University School of Medicine, in Durham, North Carolina, and his colleagues examined the quantity of B cells in blood samples or gut lymph nodes taken from 26 recently infected people. B cell levels in blood were measured 17 days after infection in 26 people, and in gut tissue 47 days after infection in 14 people. Some of the patients had started antiretroviral (ARV) therapy right away, while others had not. Patient samples in both groups were compared with samples taken from HIV-negative study participants.

Just 17 days after infection, Levesque’s team found signs of significant B cell damage. The number of naive B cells in HIV-infected patients was half that in HIV-negative patients. Naive cells are critical, because they can be educated to respond to a new organism that enters the body, such as HIV.

After 47 days of infection, there was also significant damage to three groups of cells in gut lymph nodes (called Peyer’s patches)—follicular dendritic cells, CD4 cells and B cells, all of which must work together to mount a necessary antibody response. Moreover, Levesque’s group found, the higher a person’s viral load, the more likely he or she was to have damaged lymph nodes.

The authors hypothesize that HIV might cause much of the observed damage by overactivating the immune system. Designed to kill foreign invaders, the immune system may turn on itself and cause cells to die prematurely, faster than new cells can adequately replace them. The authors also comment that their study may influence research into vaccines, most of which are designed to stop or control infection through antibodies.