Changes in co-receptor-use by human immunodeficiency virus type 1 (HIV-1) strains are relatively rare in vivo. Here we describe two variants derived from the CCR5-using strain SF162, selected for replication in the C8166 T-cell line. Amino acid substitutions in the V3 loop conferred CXCR4-use; however, the loss of macrophage-tropism by one variant was due to a single mutation in the start codon of vpu. We discuss how V3 loop and vpu mutations acquired by replication in T-cell lines in vitro correlate with similar changes reported for primary isolates and HIV-1 sequences in vivo.

译文

人类免疫缺陷病毒1型 (HIV-1) 菌株在体内共同使用受体的变化相对罕见。在这里,我们描述了源自CCR5-using菌株SF162的两种变体,选择用于在C8166 T细胞系中复制。V3环中的氨基酸取代赋予了CXCR4-use; 然而,一个变体的巨噬细胞嗜性丧失是由于vpu起始密码子中的单个突变所致。我们讨论了在体外T细胞系中通过复制获得的V3环和vpu突变如何与体内原代分离株和HIV-1序列报道的类似变化相关。

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