Somatic recombination in b-cells and t-cells is essentially a numbers game, leading to a variety of b-cell receptors and consequently antibodies. When one of those b-cells recognizes an epitope which belongs to a pathogen, it's pure coincidence, and only after that the clonal expansion and antibody production of this specific cell is initiated.

That's why the search for neutralizing antibodies for SARS-COV-2 still continues, because new types of neutralizing antibodies are still found in patient sera, which might be more potent in preventing severe disease.

To answer briefly: The chance that two people produce the same antibody (ies) is non-zero but rather low. How effective in neutralizing an antibody is depends on a lot of things, pure chance being the most important.

Short answer: no, they do not produce the same antibodies/immune response.

Somatic Hypermutation is not the only thing here but is one reason for this. The other reason is: T cells are actived in response to antigen being presented on cells with a so called Major Histogompatibility Complex (MHC). The antigen is not presented as a whole but rather smaller parts of it (peptides) are presented on MHC. You inherit the genes for MHC from your parents and the type of MHC that you have determines which antigen peptides can be presented on your cells.

This means that people with different MHC present different parts of an antigen to T cells which results in T cells with different receptors being activated.

Some peptides seem to be more crucial/important for a defense against a pathogen. This also means that some people are better in defending themselves against some pathogens because they can present those peptides that are more important. However, there's no type of MHC that is overall better for defense agains all different types of pathogens.

There exist thousends of genes for MHC in the human population. The reason for this might be that having many different allels and thus MHC complexes in a population makes it very hard for any one pathogen to eliminate a whole population since there probably will always be a part of the population that can defend themselves very well agains the parhogen.

My background: I'm a bioinformatics student and have had several courses about Immunology.

Depends. The body creates antibodies towards more or less specific parts of surface molecules, the antigens. Now if your body manages to create antibodies that are found on both pathogens, they will both be subjected to the immune respone. There are antibodies more specific, so only a certain type of antigen can be adhered to, while other antibodies will attach to almost anything.

Now if person A develops antibodies that have a higher affinity to a antigen than person B, theirs will be more effective at binding pathogens. But there are so many more parameters to check that this alone is not enough to effectively fend off illnesses.

Other people have answered correctly but the details are interesting (and I’m sitting in an airport waiting for my plane to arrive so I have time).

In the big picture, people generally produce “the same” antibodies in that almost everybody tends to target the same places on a pathogen protein. For example, H1N1 influenza viruses have 6-7 places that antibodies preferentially bind to, and different people all target those same places. They’re called “immunodominant” sites, and immunodubdominant sites are less well targeted.

(Because this is biology, nothing is ever 100%, so there are occasionally people who don’t target one or a few sites well, or people who are particularly good at targeting sites that are normally subdominant. Studying these people and understanding why they do this is an active area of research.)

So that’s the big picture, but if you drill down and look at the actual protein sequence of the antibodies that are doing the binding, they are not typically the same. Other comments have pointed to somatic hypermutation as a cause of this, but even ignoring SHM, most people have very different sets of responding antibodies. Antibodies are originally generated randomly, and it turns out that there are many ways to find very similar solutions - there may be billions of ways to get an antibody that binds to H1N1 immunodominant site “Sa”, say.

So if you compare the sequences of antibodies that are apparently doing the same thing - even between identical twins infected with the same virus at the same time - you won’t find much overlap.

But, drilling down yet another level, you will find some some overlap. We call the overlapping sequences, that are shared between different people, “public” sequences, and those that are not shared “private”.

The ability to sequence antibodies in this way is fairly new, with tech that really started to become widespread in the last ten years, so we are still trying to get a handle on the ratio of public to private sequences. If you look at two people, they may share no sequences; if you look at 100, you may find a couple dozen clusters that various people share; if you look at a thousand, who knows? It’s starting to seem that a significant percentage of antibodies are kind of public - someone else out there has something like it; but most are not widely public - it might only be shared among say 5% of the population.

Again, this is an area of very active research, with groups trying to understand the significance and potential uses of public vs private sequences.

It’s more complex than it looks like. The body randomly creates many different antibodies against many different type of antigens. The one that’s able to bind on the antigen on the virus is the one that will start reproducing and creating millions of itself if necessary to fight the specific virus.

The two antibodies of the two different persons will be most likely be different. One of them will probably have a higher affinity towards the virus compared to the other person which will mean that that person may also fight the virus faster.

I can’t go into much more detail since I still haven’t been taught much about this topic yet.

Source: med student

Thank you everyone for the detailed responses!

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Not identical but likely attacking similar parts of the microbe. Also keep in mind when you get infected you have a polyclonal antibody response which basically means a bunch of different antibodies attacking different antigens or spots. Collectively they will work pretty similarly but the individual antibodies are not likely to be exactly the same even when they are targeting the same spot.