"The research supports a new role for B cells in the development and spread of HIV between cells, with important implications for future studies and drug development efforts that focus on reservoirs of HIV in cells other than T cells," said Charles R. Rinaldo, Jr., Ph.D., professor and chairman of the department of infectious diseases and microbiology at Pitt's Graduate School of Public Health (GSPH) and the study's senior author.
Nearly all approved HIV drug regimens and most of those being tested in clinical trials focus on T cells of the immune system, where HIV replicates and thrives. HIV hijacks T cells by binding to a cell membrane molecule called CD4 and to either or both of two other receptors, from which the two strains of HIV, X4 and C5, take their names. Once anchored on the membrane, it's able to slither inside and take command of the cell. But as the Pitt studies have found, there is an important first step in a new pathway involving B cells that express a protein called DC-SIGN. B cells are key players in an immune response.
While these cells themselves do not become infected, they play a pivotal role as an accomplice in HIV's takeover of T cells.
According to the research to be reported by Giovanna Rappocciolo, Ph.D., research assistant professor of infectious diseases and microbiology at GSPH, laboratory studies provide evidence of DC-SIGN in subsets of B cells from both healthy subjects and HIV infected individuals and indicate DC-SIGN is both a point of entry for HIV and necessary for T cell infection.
B cells were isolated from blood samples obtained in 33 healthy subjects and 20 adult patients with HIV from the Mul
Source:University of Pittsburgh Medical Center