Protection against retroviruses are owing to a different form of immunity. An RNA-based molecular immunity hypothesis.
Protection against retroviruses are owing to a different form of immunity. An RNA-based molecular immunity hypothesis.
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针对逆转录病毒的保护是由于不同形式的免疫。
DOI：
10.1097/00129039-200006000-00008
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Amjad,M
中科院分区：
文献类型：
--
作者：
Bagasra,O;Amjad,M
在科学研究的过程中，有时会出现与现有理论不一致的数据。然而，当旧理论似乎仍然可行时，科学家们天生就不愿意接受新思想，即使它们需要修改或更新。通常，这种科学沉默的后果只是在学术会议或学术期刊上活跃了辩论。然而，在人类免疫缺陷病毒1（HIV-1）发病机理领域，在理解逆转录病毒感染的基本生物学方面长达15年缺乏进展的影响可以用人类的术语来衡量--到目前为止，实际上可能有4000多万人感染HIV-1，到新千年来临时，这一数字将增加到1亿。如果不能迅速取得进展，许多HIV-1感染者可能会死于获得性免疫缺陷综合征（AIDS）及其并发症。有效的治疗方法必须在分子水平上发挥作用，因为这是逆转录病毒发挥作用的规模，并且迫切需要针对HIV-1的有效疫苗，因为该流行病在全球范围内持续蔓延[1]。有效治疗和疫苗的线索一直摆在我们面前，但传统智慧在科学调查期间一再误导我们。例如，就在5年前，大多数科学家认为HIV-1感染包括一个很长的潜伏期，在此期间很少或没有病毒活性。我们现在知道，这个假设可能是不正确的，由此产生的调查路线导致死胡同（2）。更糟糕的是，观察到的事实和流行理论之间的不一致导致了在艾滋病病原体的徒劳争论上花费大量资金-在压倒性的数据无可争议地表明HIV-1是疾病的原因之后很久。“HIV-AIDS假说”的反对者已经提出了一些有效的观察，特别是涉及到明显影响HIV-1发病过程的各种“辅助因子”（3），然而主流科学家似乎把更多的精力集中在对反对者的震惊上，而不是试图在他们的论点中检查和适应真理的核心。现有的免疫学理论使得这些异议者的概念以及相当数量的其他数据（即猴免疫缺陷病毒（SIV）的减毒活疫苗株，流行病学和实验室数据）非常困难。
In the course of scientific investigation, data sometimes emerge that cannot be readily reconciled with existing theory. Yet scientists by nature are reluctant to accept new ideas when the old theories still seem viable, even when they are in need of revision or update. Usually the consequences of this scientific reticence are simply enlivened debates at academic conferences or in scholarly journals. However, in the field of human immunodeficiency virus 1 (HIV-1) pathogenesis, the effect of a decade and half-long lack of progress in understanding the fundamental biology of the retroviral infection can be measured in human terms—literally more than 40 million people may be infected with HIV-1 by now, and this number will increase to 100 million by the dawn of the new millennium. Many of HIV-1 infected individuals will likely die from acquired immunodeficiency syndrome (AIDS) and its complications if rapid progress is not made. Effective treatments must be developed that work at the molecular level because that is the scale on which retroviruses function, and an effective vaccine for HIV-1 is desperately needed because the epidemic continues to expand worldwide (1).Clues to effective treatment and vaccine have long been before us but conventional wisdom has repeatedly misguided us during scientific investigation. Just 5 years ago, for example, most scientists thought that HIV-1 infection included a long latency period in which there was little or no viral activity. We now know that this hypothesis may be incorrect and that resulting lines of inquiry lead to blind alleys (2). Worse still, inconsistencies between observed facts and prevailing theory have led to the expenditure of considerable capital over a futile argument over the etiologic agent of AIDS—long after overwhelming data have incontrovertibly shown HIV-1 to be the cause of the disease. The dissenters of the “HIV-AIDS hypothesis” have made some valid observations, particularly involving the various “cofactors” that clearly influence the course of HIV-1 pathogenesis (3), yet mainstream scientists seem to have focused more energy on being appalled by the dissenters than on trying to examine and accommodate the kernels of truth in their arguments. Existing immunologic theory makes the accommodation of these dissenters' concepts as well as considerable quantities of other data (ie, live attenuated vaccine strains of simian immunodeficiency virus (SIV), epidemiologic and laboratory data) exceedingly difficult.
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影响因子：
158.5
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影响因子：
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作者：
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