Figure 3
Figure 3. Proviral nef sequence analysis of the cases. (A) nef sequences obtained from C1 to C3 are aligned with the clade B consensus sequence. Dots indicate identity with the consensus sequence; dashes, gaps; and asterisks, stop codons. Sequence variations in C1 and C2 occurred in regions of common length polymorphisms. Premature stop codons occurred in all 5 sequences obtained from C3 and were not due largely to G to A hypermutation. (B) A phylogenetic tree of nef sequences from 3 cases (C1, ×; C2, †; C3, ★) and other chronically infected patients from another study (M.S., personal communication), including conventional LTNPs/ECs (black circles), viremic progressors (solid black upward turning arrow heads), and Rx<50 (solid black downward turning arrow heads) was constructed for each patient by classic, maximum-likelihood and Bayesian methods. Other clade subtype nef sequences are included for comparison.

Proviral nef sequence analysis of the cases. (A) nef sequences obtained from C1 to C3 are aligned with the clade B consensus sequence. Dots indicate identity with the consensus sequence; dashes, gaps; and asterisks, stop codons. Sequence variations in C1 and C2 occurred in regions of common length polymorphisms. Premature stop codons occurred in all 5 sequences obtained from C3 and were not due largely to G to A hypermutation. (B) A phylogenetic tree of nef sequences from 3 cases (C1, ×; C2, †; C3, ★) and other chronically infected patients from another study (M.S., personal communication), including conventional LTNPs/ECs (black circles), viremic progressors (solid black upward turning arrow heads), and Rx<50 (solid black downward turning arrow heads) was constructed for each patient by classic, maximum-likelihood and Bayesian methods. Other clade subtype nef sequences are included for comparison.

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