Now, most of these point mutations are harmless.

现在，大多数这些点突变都是无害的。

Most of these gene mutations are deletions or duplications of one or more exons, and a small amount are point mutations.

基因突变大多数为一个或多个外显子的缺失或重复，小部分是点突变。

But every now and then, a point mutation disrupts an important capability in a cell or causes a cell to misbehave in harmful ways.

但有时，点突变会破坏细胞的重要功能，或导致细胞以有害的方式出现行为失常。

Millions suffer from sickle cell anemia because they have a single A to T point mutations in both copies of their hemoglobin gene.

数百万人患有镰状细胞性贫血，因为他们的血红蛋白基因的两个拷贝都有一个A点到T点的突变。

But I saw the lack of a way to fix point mutations, which cause most human genetic diseases, as a major problem standing in the way.

但我看到缺乏一种，导致大多数人类遗传疾病点突变的修复方法，这是一个阻碍的主要问题。

Grievous genetic diseases caused by point mutations are especially frustrating, because we often know the exact single-letter change that causes the disease and, in theory, could cure the disease.

由点突变引起的严重遗传性疾病尤其令人沮丧，因为我们通常知道引起该疾病的确切的单字母变化，并且理论上该疾病可以治愈。

Throughout the history of medicine, we have not had a way to efficiently correct point mutations in living systems, to change that disease-causing T back into a C.

纵观整个医学史，我们还没有办法有效地纠正生命系统中的点突变，将这种引起疾病的T转变为C。

But correcting the largest fraction of disease-causing point mutations would require developing a second class of base editor, one that could convert As into Gs or Ts into Cs.

但是纠正最大部分的致病点突变需要开发第二类碱基编辑器，它可以将 As 转化为 Gs 或将 Ts 转化为 Cs。

But for most point mutations that cause genetic diseases, simply cutting the already-mutated gene won't benefit patients, because the function of the mutated gene needs to be restored, not further disrupted.

但是对于大多数导致遗传疾病的点突变来说，仅仅切割已经突变的基因对患者没有好处，因为突变基因的功能需要恢复，而不是进一步破坏。

Throughout the history of medicine, we have not had a way to efficiently correct point mutations in living systems, to change that disease-causing T back into a C. Perhaps until now.

纵观医学史，我们一直没有办法有效地纠正生命系统中的点突变， 将导致疾病的 T 变回 C。 也许直到现在。

Among the more than 35,000 known disease-associated point mutations, the two kinds of mutations that this first base editor can reverse collectively account for about 14 percent or 5,000 or so pathogenic point mutations.

在已知的35000多个疾病相关点突变中，这两种第一碱基编辑能逆转的突变共占致病点突变的14%或5000左右。

While base editors are too new to have already entered human clinical trials, scientists have succeeded in achieving a critical milestone towards that goal by using base editors in animals to correct point mutations that cause human genetic diseases.

虽然碱基编辑太新了，还不足以进入人类临床试验，但科学家们已经成功地实现了这一目标，即在动物身上使用碱基编辑来纠正导致人类遗传病的点突变。