抗体産生の減少率と長期免疫との関係


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感染後2〜3か月で抗体産生が低レベルであることを示すCOVID-19記事が多数あります。彼らはすべて、感染が長期的な免疫を提供しない可能性があることを示す指標であることを指摘しています。しかし、抗体産生のこの減少が長期免疫の可能性の低下と相関する理由について説明されたメカニズムを見たことはありません。免疫系についての私の(限られた)理解は、いつ抗体を産生すべきかを特定することが仕事であるメモリー細胞があり、それらが長期免疫にとって重要なことであるということでした。結局のところ、抗体を作るにはエネルギーが必要です!

抗体の低下と長期免疫との間のこの関係は十分に定着しているようです。感染後の抗体の低下が長期免疫の可能性が低いことを示す理由を説明するために、これまでにどのようなメカニズムが見られましたか?

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The primary immune response (when you first get exposed) is different from the secondary (from the memory cells). In the primary response, different antibodies are used (mostly IgM). The secondary immune response mostly uses IgG antibodies. This secondary response is stronger and antibodies are detected for longer.

The term primary and secondary are slightly misleading in the sense that even in the first exposure to a disease you will develop a secondary response as highlighted in the nice graph below from this nice article.

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I do not know the articles you read but one I have seen in nature described the phenomenon that the IgG antibodies (those from the secondary response) decline much quicker and patients become seronegative (they do not have any antibodies left in their blood serum) very quickly. They only looked at the antibody levels so did not try and explain why this is happening. But they found that the immune response is much stronger in patients with symptoms compared to those without symptoms. This makes sense as the immune system needs a so-called secondary signal (inflammation etc.) to start an immune response otherwise it would constantly attack your own cells. This secondary signal is most likely much weaker if you do not have symptoms.

Their conclusion is:

The reduction in IgG and [..] antibody levels in the early convalescent phase might * have implications for immunity strategy and serological surveys. *(I have added the emphasis)

The reasoning I believe for the statements in the press that COVID might not cause immunity is that the low levels of IgG antibodies in the first exposure event might indicate the secondary immune response could not be sufficient to achieve immunity. Reasons could be that not enough Memory-cells are made or these are not as effective as they should be. But only time will tell. I would suspect that the immunity will heavily depend on whether a patient did show symptoms (had a strong second signal to the immune system) or not.

PS. (Just in case...) This does not mean a possible vaccination will be less effective than an actual infection because generally, these do not cause symptoms. In that case of vaccines so-called adjuvants deliver the second signal and inflammation etc. is not needed.