There are two types of immune systems in the body—innate and adaptive/acquired—to protect against pathogens or harmful substances. Innate protection is a very thick scar system. Instead of specifically addressing each threat in a different way, it tends to work in much the same way.

Prevention of dengue

For example: If a molecule or molecule with a barrier pattern identified as dangerous and larger than a certain size is found, dendritic cells digest it by phagocytosis. Not so much judgment about what that thing actually is and what kind of risks it might have, or whether it's okay to eat it at all, or how to better deal with it in the future.

On the other hand, acquired security systems offer different specialized solutions for different risks. This system, which first emerged in organisms of the order Chondrichthyes (i.e. cartilaginous fish with jaws such as sharks) about 400 million years ago, is dependent on pre-existing innate defense mechanisms.

For example, when a dendritic cell digests something, it attaches small pieces of that thing (antigen) to the outside of its own cell membrane and puts on a show. This is called antigen presentation.

A cell of the acquired immune system, such as a lymphocyte, can be stimulated to bind to a specific protein on its cell membrane with the presented fragment and initiate a specific defense against the original carrier of the fragment. Our body's acquired immune system can recognize approximately one million to one billion (107–108) of these different antigens and respond to each of them individually.

Each type of antigen requires at least the same number of proteins to make a specific connection. And each type of protein requires at least one gene to signal its production. But the number of human genes is like twenty thousand!

Susumu Tonegawa of Japan won the Nobel Prize in medicine in 1987 for solving this problem. He showed that tiny genes can assemble together to signal the production of millions of different proteins. Lymphocytes are one of the cells of acquired immunity. When born, these genes are shuffled around on a fairly random basis.

Therefore, only a few (10-1000) lymphocytes produce proteins that bind to a particular antigen. For B-lymphocytes and T-lymphocytes, that protein is called antibody and T-cell receptor (TCR), respectively. It may be that the antigen has never been exposed to in life, or that there is no antigen in nature that binds to that antibody or TCR.

But what if an antigen enters the body that is 'common' on the lymphocyte's syllabus? That is, if it has the ability to bind specifically to one of the millions of types of antibodies or TCRs, the few lymphocytes containing that particular protein start to multiply. The antigen then begins to attack its carrier.

In the case of dengue virus, attack basically means two things. First, antibodies that bind to the E and pre-M proteins of the dengue virus can be used to mask the virus. As a result, it cannot enter any new cells.

Because those proteins are the key to enter the virus cell. If the shape of that key changes, it will no longer work. Second, the T-lymphocyte's appropriate TCR engagement with NS1 antigen-presenting cells destroys that cell. Because, the dengue virus must be buzzing inside the stomach of the NS1-carrying cell. Otherwise NS1 will come from where! That is why it is not detectable in blood test after three to four days of dengue fever. Because, NS1-bearing cells are destroyed in it.