Interleukin-16 (IL-16) inhibits human immunodeficiency virus replication in cells from infected subjects, and serum IL-16 levels drop with disease progression

The role of recombinant interleukin-16 (rIL-16) in regulating human immunod eficiency virus type 1 (HIV-1) replication in endogenously infected cells h as been investigated. Cultures of CD8 cell-depleted mitogen-activated lymph ocytes from 22 of 26 HIV-1-infected subjects presented variable levels of s ecreted p24 antigen. The presence of rIL-16 throughout the 14-day culture p eriod dramatically inhibited p24 release into the culture supernatants. Thi s effect was found to be mediated through inhibition of viral transcription but to be independent of the induced levels of other cytokines or chemokin es known to regulate viral replication. Analysis of serum samples from HIV- l-infected subjects over a period of 8 years showed maintained or even incr eased IL-16 levels during the whole asymptomatic phase and a significant dr op on progression to disease. These results strongly support a potential th erapeutic value of rIL-16 in HIV-1 infection and the use of serum IL-16 lev els to monitor disease progression.