Immunity comes in many forms when dealing with pathogens, cancers and other foreign invaders. It’s important to understand the rudimentary immune response to a foreign invader in order to fully appreciate how complex and vital is the human immune system.

The Basics:

Immunity is multilayered and comes in two forms; Innate Immunity and Adaptive immunity (also referred to as acquired immunity).

Innate immunity is the first to be mobilized once a foreign invader is recognized. There are Physical Barriers such as skin, eyelashes, nasal cilia, and the GI tract, Defense Mechanisms such as mucous, bile, saliva, tears and sweat and General Immune Responses such as inflammation which is initiated on a cellular level through something called the complement cascade which seeks to destroy the invader through phagocytosis.

Innate immunity lacks specificity. In other words, it seeks to neutralize anything foreign that is not made inside the body, but it lacks specificity on what that outside invader is. That is where Adaptive Immunity comes in. Adaptive Immunity, or Acquired Immunity, uses specific antigens (foreign invader) to mount an antibody response. Exposure to bacteria, fungi, viruses and other pathogens allow the adaptive immune system to build its memory database for present and future use. This stage of the response is slower than the innate response which is why the two work together to keep the host safe and functioning. Counter to the many cells and systems involved in the innate response, acquired immunity relies on 2 cell lines originating from the bone marrow, T cells and B cells.

B-cells mature within the Bone marrow.  Memory B-cells or Plasma cells.  When naive B-cells emerge, they are armed with many surface antibody receptors scouring the host looking for antigens (keys) that fit the receptors (locks) and when they match, it signals cell proliferation of plasma cells to secrete specific antibodies which can bind directly to that particular invader with the intent to neutralize its pathogenicity.

T-cells remain immature in the bone marrow and migrate to the Thymus for maturation where they express either CD4 or CD8 receptors (not both). For simplification purposes, these receptors aid in recognizing antigens bound to specific Macrophages or Dendritic cells for the purpose of recognition, activating B cells and removing them along with infected host cells. (T-regulatory CD4, T-helper CD4 and T-cytotoxic CD8, respectively).

Innate Immunity vs. Adaptive Immunity: A summary

Now that you have a basic understanding of the immune system, you can appreciate the complexity involved in fighting disease. It is known that immunity can last a lifetime, but often, the memory of certain antigens may fade. For this reason, booster shots are recommended for some pathogens. The question is, are they necessary?

Long-lasting immunity depends on the makeup of each person, their exposure in the interim and their overall health. For this reason, it is often prudent to have an antibody titer for that particular pathogen analyzed. For example, I received a Hepatitis B vaccine in the 1980’s. It was recommended many times since that I get a booster. Instead, I opted to run a titer to see if I still have effective antibody concentrations rather than challenge my body with more antigen. Without fail, my HBV-IgG remains quite high indicating that if I am exposed to the virus, I will neutralize it without incident.

During the current pandemic, it has been hypothesized that immunity for SARS CoV2 is short lived which prompted me to do some digging. After identifying several subjects with previous SARS 1 infections, T cell and B cell analysis was performed only to show that 17 years later, they still have the capability to recognize and neutralize the virus. Additionally, there is no documented case of a SARS1 patient becoming infected with SARS2.

“We know that people who were infected with the first SARS coronavirus, which is the most similar virus to SARS-CoV-2, are still seeing immunity 17 years after infection.”

Nikolich-Zugich, Bhattacharya

This prompted me to check on myself. I recovered from COVID (the infectious disease caused by SARS CoV2) in October 2020. Thus far, my IgG two weeks following infection was at 28.8 using ECLIA assay. Currently it sits at the 29 level. I think this bodes well for long-term immunity. This doesn’t account for T-cell cross reactivity or recognition, either. It is stated that often, T-cells are more than enough to neutralize SARS CoV2 infection. So many signs point to long term protection and recognition that one must wonder. Is it worth taking an experimental therapy for something with a high survivability rate and long-term recognition by one’s natural immunity?

Much like my occasional HBV titer, I think I will continue to monitor my own immune status before taking the jab.

Editor’s note: This article is a Reprint, first published on 17 May, 2021. To find out why we reprint older literature related to the Covid pandemic, read more here.