Long-term changes of serum chemokine levels in vaccinated military personnel

Significantly increased levels of macrophage inflammatory protein 1α (MIP-1α), MIP-1β and interleukin 8 (IL-8) were detected. Since these cytokines are known to have anti-human immunodeficiency virus (HIV) activity, we tested the effect of serum from these individuals on HIV-1 infectivity and susceptibility of their peripheral blood mononuclear cells (PBMCs) to HIV-1 infection in vitro. Sera from vaccinated military personnel inhibited, and their PBMCs were partially resistant to, infection by HIV-1 strains tropic to CCR5 (R5), but not to CXCR4 (X4), chemokine receptor.These findings demonstrate that increased anti-HIV chemokines can be detected in vaccine recipients up to 68 weeks following immunization.Viruses and other pathogens express a variety of proteins interfering with the host immune responses to counteract immune surveillance and increase their virulence [1]. The ability of a pathogen to modulate host response to infection and the reaction of host cells to such immunomodulation form an environment that can influence concurrent or subsequent infections by other pathogens [2-5]. A significant role in this immunomodulation is played by the cytokine-chemokine network [6]. For example, infection with mouse lymphocytic choriomeningitis virus abolishes replication of the hepatitis B virus, and this process is mediated by tumor necrosis factor-α and interferon-γ [7]. Co-infection of human lymphoid tissue ex vivo with human herpesvirus 6 and CCR5-utilizing HIV-1 results in suppression of HIV infection, a process dependent on herpesvirus 6-mediated upregulation of CC chemokine regulated upon activation in normal T cells expressed and secreted (RANTES), a natural ligand for CCR5 [8]. Upregulation of chemokines was also implicated as a primary mechanism of HIV-1 suppression caused by at least two other pathogens – measles [9] and GB virus C (GBV-C) [4]. Similar to co-infections, immunizations, especially with live vaccines, can change the immune environment and cytok