Bayoumi R A
Med Hypotheses. 1987 Mar;22(3):287-98. doi: 10.1016/0306-9877(87)90193-9.
It is proposed that the in vivo mechanism of protection against falciparum malaria in individuals of the Hb AS genotype is not due solely to the adverse influence of Hb AS erythrocytes on the intraerythrocytic growth and development of P. falciparum. Instead, the simple physiological effect of Hb S on parasite growth appears to trigger an in vivo process of enhancement of the intensity and/or specificity of the host immune response, leading to acquired protective immunity, in a process simulating vaccination. Testing the hypothesis may lead to the identification of plasmodial antigens that induce protective responses in the human host and distinguish them from non-protective, immunosuppressive or decoy antigens that promote parasite survival. This may ultimately help in the selection of candidate antigens for a malaria blood-stage vaccine.
有人提出，Hb AS基因型个体对恶性疟原虫的体内保护机制并非仅仅归因于Hb AS红细胞对恶性疟原虫红细胞内生长和发育的不利影响。相反，Hb S对寄生虫生长的简单生理效应似乎触发了一个体内过程，增强宿主免疫反应的强度和/或特异性，从而在模拟疫苗接种的过程中产生获得性保护性免疫。对这一假设进行测试可能会导致识别出能在人类宿主中诱导保护性反应的疟原虫抗原，并将它们与促进寄生虫存活的非保护性、免疫抑制性或诱饵抗原区分开来。这最终可能有助于选择疟疾血液阶段疫苗的候选抗原。
