Schønning K, Bolmstedt A, Novotny J, Lund O S, Olofsson S, Hansen J E
Laboratory of Infectious Diseases, Department 144, Hvidovre Hospital, Denmark.
AIDS Res Hum Retroviruses. 1998 Nov 1;14(16):1451-6. doi: 10.1089/aid.1998.14.1451.
An N-glycan (N306) at the base of the V3 loop of HIV-BRU gp120 is shielding a linear neutralization epitope at the tip of the V3 loop on oligomeric Env. In contrast, this epitope is readily antigenic on monomeric gp120. Immunization with recombinant monomeric HIV-BRU gp120 may thus be expected to elicit antibodies preferentially neutralizing mutant variants of HIV-BRU lacking the N306 glycan. Therefore, two guinea pigs were immunized with monomeric wild-type HIV-BRU gp120 possessing the N306 glycan and immune sera were tested for neutralization against target viruses HIV-BRU, -A308, and -A308T321. HIV-A308 and HIV-A308T321 lack the N306 glycan; HIV-A308T321 contains an additional mutation at the tip of V3 rendering it resistant to MAb binding at this epitope. Both immune sera preferentially neutralized the two mutant virus variants lacking the N306 glycan, with a 10- to 20-fold increase in neutralization titer compared with the wild-type HIV-BRU. Thus, immunization with monomeric HIV-BRU gp120 elicited antibodies preferentially neutralizing HIV variants lacking the N306 glycan. In addition to antibodies directed against the tip of V3, other antibodies directed against epitopes shielded by the N306 glycan on the envelope oligomer were elicited by the immunization, as demonstrated by the ability of the immune sera to neutralize HIV-A308T321. One such epitope was overlapping the NEA-9284 epitope located at the amino-terminal flank of the V3 loop. Our results demonstrate that monomeric gp120 contains immunogenic structures inaccessible on the envelope oligomer. The limited ability of recombinant gp120 vaccines to induce neutralizing antibodies against primary isolates may thus not exclusively reflect genetic variation.
HIV-BRU gp120的V3环基部的一个N-聚糖(N306)屏蔽了寡聚Env上V3环顶端的一个线性中和表位。相比之下,该表位在单体gp120上易于呈现抗原性。因此,用重组单体HIV-BRU gp120免疫可能会诱导出优先中和缺乏N306聚糖的HIV-BRU突变变体的抗体。于是,用具有N306聚糖的单体野生型HIV-BRU gp120对两只豚鼠进行免疫,并检测免疫血清对靶病毒HIV-BRU、-A308和-A308T321的中和作用。HIV-A308和HIV-A308T321缺乏N306聚糖;HIV-A308T321在V3顶端含有一个额外突变,使其对该表位的单克隆抗体结合具有抗性。两种免疫血清均优先中和这两种缺乏N306聚糖的突变病毒变体,与野生型HIV-BRU相比,中和效价提高了10至20倍。因此,用单体HIV-BRU gp120免疫可诱导出优先中和缺乏N306聚糖的HIV变体的抗体。除了针对V3顶端的抗体外,免疫还诱导出了针对包膜寡聚体上被N306聚糖屏蔽的表位的其他抗体,免疫血清对HIV-A308T321的中和能力证明了这一点。其中一个这样的表位与位于V3环氨基末端侧翼的NEA-9284表位重叠。我们的结果表明,单体gp120含有包膜寡聚体上无法接近的免疫原性结构。重组gp120疫苗诱导针对原代分离株的中和抗体的能力有限,因此可能不完全反映基因变异。