Fig. 1: Immunization regimen, infection rate and SIV plasma virus.
From: Vaccine plus microbicide effective in preventing vaginal SIV transmission in macaques
a, Rhesus macaques were subdivided into four groups: vaccine (n = 18), vaccine + SAMT-247 (n = 20), SAMT-247 (n = 6), and concurrent and historical controls (n = 6 and 31). Thirty-eight animals were primed with ΔV1 DNA-SIVgp160+p57 Gag and boosted with ALVAC-SIV encoding env, gag and pol and ALVAC-SIV + ΔV1 gp120 protein in alum hydroxide at the indicated timepoints. Twelve animals remained naïve until SIV challenge. Beginning at week 17, vaccine efficacy (VE) was assessed by subjecting all animals to up to 14 weekly intravaginal viral exposures (arrows) in the presence or absence of SAMT-247 until infection was confirmed. Animals either received 0.8% SAMT-247 in HEC gel (n = 26) or HEC gel only (n = 24) 4 h before each low-dose SIVmac251 challenge. b,c, Significant protection in the vaccine group (P = 0.0074) (b) and the vaccine + SAMT-247 group (P < 0.0001) (c) compared with concurrent + historical controls. d, Delayed SIV acquisition in the vaccine + SAMT-247 group compared with the vaccine-only group (P = 0.006). e, No differences in delayed acquisition in the SAMT-247 group were observed compared with the combined concurrent plus historical controls (P = 0.27). f, Viral load (VL) geometric means of all macaque groups over time. Productive infection was qualified by the presence of viral DNA and RNA in mucosa and persistence of viral RNA in plasma over time. Data shown in b–e were analysed with log-rank (Mantel–Cox) test.
