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. 2017 Nov 6;214(11):3239–3261. doi: 10.1084/jem.20162123

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© 2017 Leitman et al.

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Figure 6. — Preferential recognition of autologous TL9 variants by HIV-infected children compared with adults. (A) Development of preferential recognition of autologous TL9-Q182G variant by pediatric subject K-004-C between age 8.2 yr, at which time autologous virus encoded a mix of Q182P/Q182G variants, and 12.8 yr, at which time autologous virus encoded only the Q182G variant, by population sequencing of virus. HLA type and autologous sequence of the mother K-004-M are unknown. ELISPOT assays repeated in triplicate. (B) Development of preferential recognition of autologous TL9-Q182G variant by pediatric subject K-044-C between age 4.5 yr, at which time autologous virus encoded a mix of Q182P/Q182T variants, and 8.7 yr, at which time autologous virus encoded only the Q182G variant, by population sequencing of virus. The mother (K-044-M) was HLA-B*42:01/81:01 negative and autologous virus when sequenced at child’s age 4.5 yr encoded wild-type TL9, suggesting that wild-type TL9 was transmitted to the child. ELISPOT assays repeated in triplicate. (C) The magnitude of the IFN-g ELISPOT response to wild-type TL9 is lower than to the autologous variant among children (n = 11; mean 531 vs. 1,010 spot-forming cells per million PBMCs; P = 0.02, paired t test; P = 0.002, Wilcoxon signed-rank test). Among adults, the IFN-γ ELISPOT response to wild-type TL9 tended to be higher than to the autologous TL9 variant, although this did not reach statistical significance (n = 16; median 1,597 vs, 882 spot-forming cells per million PBMCs; P = 0.25, paired t test; P = 0.40, Wilcoxon signed-rank test). (D) Frequency of subjects showing preferential recognition of autologous variant is significantly higher in pediatric subjects than adult subjects (10/11 = 91%; vs. 5/16 = 31%; P = 0.0047, Fisher’s exact test). SFC, spot-forming cell.