Corley P A
Med Hypotheses. 1995 Jun;44(6):483-9. doi: 10.1016/0306-9877(95)90511-1.
Recent evidence suggests that HIV infection and the clinical and laboratory manifestations of acquired immunodeficiency syndrome (AIDS) are a result of the genetic influence of the virus on cellular adrenocorticotrophic hormone (ACTH) and cortisol metabolism. Recent genetic studies substantiate this view with the observation that the HIV-1 genome is linked to glucocorticoid inducibility and to glucocorticoid receptor binding, and may explain the strong ability of cortisol to enhance HIV replication. Adrenocortical hyperactivity observed in HIV-infected individuals has been found to be independent of the hypothalamic-pituitary axis, and is apparently a result of increased ACTH production by HIV. It is proposed that the HIV-induced cortisol excess is the foundation of the immunosuppression seen in AIDS, and is the basis for alternative avenues of treatment, including the use of ascorbic acid.
最近的证据表明，HIV感染以及获得性免疫缺陷综合征（AIDS）的临床和实验室表现是该病毒对细胞促肾上腺皮质激素（ACTH）和皮质醇代谢的基因影响所致。最近的基因研究证实了这一观点，观察发现HIV-1基因组与糖皮质激素诱导性以及糖皮质激素受体结合有关，这可能解释了皮质醇增强HIV复制的强大能力。在HIV感染个体中观察到的肾上腺皮质功能亢进与下丘脑-垂体轴无关，显然是HIV导致ACTH分泌增加的结果。有人提出，HIV诱导的皮质醇过量是AIDS中免疫抑制的基础，也是包括使用抗坏血酸在内的替代治疗途径的基础。
