And identifying reinfections, as opposed to prolonged viral shedding , remains a challenge. Now, sufficient time has passed since the beginning of the pandemic and the deployment of vaccines to finally assess long-term protection as it relates to natural and vaccine-induced immunity. Researchers in Israel compared the rates of infection after vaccination — called breakthrough infection — with the rates of reinfection.
The database includes extensive demographic data, clinical measurements, outpatient and hospital diagnoses, and comprehensive laboratory data. The study population included people who were at least 16 years old and fell into one of three categories:. The analysis indicated that people who had never had the infection and received a vaccine in January or February of were up to 13 times more likely to contract the virus than people who had already had the infection.
The researchers also compared reinfection rates among people who had once had a confirmed SARS-CoV-2 infection and were still unvaccinated and people who had once had the infection and had also received one dose of the Pfizer-BioNTech vaccine.
Results showed that the unvaccinated group was twice as likely to contract the infection again, compared with those who had received one dose of the vaccine. The findings appear to indicate increased protection from natural immunity over vaccine-conferred immunity.
This may be due to a more extensive immune response to the SARS-CoV-2 proteins, compared with the immune activation provided by the vaccine, the researchers suggest. Infection disease experts warn that the findings should not be viewed as an excuse to forego vaccination.
In an interview with MNT , Dr. William Schaffner , a professor of infectious diseases at Vanderbilt University Medical Center, in Nashville, TN, said that the vaccines are doing exactly what they were designed to do. The researchers behind the new study acknowledge several limitations. Since the Delta variant was dominant during the study period, the findings concerning natural immunity may not apply to infections with other variants of SARS-CoV Other limitations include a possible underestimation of asymptomatic infections, as these cases are often not tested or recorded.
There are two types of adaptive immunity: active and passive. Active Immunity - antibodies that develop in a person's own immune system after the body is exposed to an antigen through a disease or when you get an immunization i. This type of immunity lasts for a long time. Passive Immunity - antibodies given to a person to prevent disease or to treat disease after the body is exposed to an antigen. Passive immunity is given from mother to child through the placenta before birth, and through breast milk after birth.
It can also be given medically through blood products that contain antibodies, such as immune globulin. This type of immunity is fast acting but lasts only a few weeks or months. How vaccines work with the immune system Vaccines provide active immunity to disease. Here is how a vaccination works: The vaccine is administered. It contains antigens to a specific disease. The immune system identifies the antigens in the vaccine as foreign invaders.
The immune system then develops antibodies to neutralize the antigens. The immune system stores these antibodies for future use in case the person is ever exposed to the disease.
NIH: Vaccine Benefits. A PDF reader is required for viewing. The alternative or properdin pathway is triggered by the deposition of complement protein, C3b, onto microbial surfaces and does not require antibodies for activation. The third pathway, the lectin pathway, is triggered by the attachment of plasma mannose-binding lectin MBL to microbes and does not require antibodies for activation.
These three pathways merge into a common pathway which leads to the formation of the membrane attack complex that can form pores in the membrane of targeted cells. The complement pathways are also integral in the opsonization or increased susceptibility of particulate antigens to phagocytosis and in triggering a localized inflammatory response.
The inflammatory response is another essential part of the innate immune response. The inflammatory response is the body's reaction to invasion by an infectious agent, antigenic challenge, or any type of physical damage. The inflammatory response allows products of immune system into area of infection or damage and is characterized by the cardinal signs of redness, heat, pain, swelling, and loss of function.
In addition to the anatomic and physiologic mechanisms, there are also Pattern recognition receptors or PRRs which contribute to the innate immune response. Pattern recognition receptors are not specific for any given pathogen or antigen, but can provide a rapid response to antigens.
PRRs are classified as membrane proteins because they are associated with the cell membrane; and, they can be found in all the membranes of the cells in the innate immune system. Although there are several hundred varieties, all the genes of the PRRs are encoded in the germline to ensure limited variability in their molecular structures.
These antigens are produced by microbal cells and not by human cells. Finally, the mononuclear phagocytes and granulocytic cells are also important to the innate response and help link the innate immune response to the adaptive immune response. Mononuclear phagocytes include monocytes which circulate in the blood and macrophages which are in the tissues. Monocytes and macrophages are highly important in antigen presentation, phagocytosis, cytokine production, and antimicrobial and cytotoxic activities.
Upon maturity of the monocytes, the monocytes circulate in the blood for approximately 8 h, then migrate into the tissues and differentiate into specific tissue macrophages or into dendritic cells. There are several types of dendritic cells which are involved in different aspects of immune functions. Many dendritic cells are important in presenting antigen to T-helper cells. However, follicular dendritic cells are found only in lymph follicles and are involved in the binding of antigen—antibody complexes in lymph nodes.
Neutrophils are highly active phagocytic cells and generally arrive first at a site of inflammation. Eosinophils are also phagocytic cells; however, they are more important in resistance to parasites. Basophils in the blood and mast cells in the tissues release histamine and other substances and are important in the development of allergies. The innate system may be able to eradicate the pathogenic agent without further assistance from the adaptive system; or, the innate system may stimulate the adaptive immune system to become involved in eradicating the pathogenic agent.
In contrast to the innate immune system, the actions of adaptive immune system are specific to the particular pathogenic agent. This response will take longer to occur than the innate response. However, the adaptive immune system has memory which means that the adaptive immune system will respond more rapidly to that particular pathogen with each successive exposure. These are the two arms of the adaptive immune system.
The B—cells and antibodies compose humoral immunity or antibody-mediated immunity; and, the T-cells compose cell-mediated immunity. As a note, natural killer cells are also from the lymphocyte lineage like B—cells and T-cells; however, natural killer cells are only involved in innate immune responses.
The first arm of the adaptive immune system is humoral immunity, functions against extracellular pathogenic agents and toxins. B—cells are produced in the bone marrow and then travel to the lymph nodes. Unlike T-cells, B—cells can recognize antigens in their native form which means that B—cells can recognize antigens without requiring that the antigen be processed by an antigen-presenting cell and then presented by a T-helper cell.
Examples of these T-independent antigens include lipopolysaccharide, dextran, and bacterial polymeric flagellin. These antigens are typically large polymeric molecules with repeating antigenic determinants. These antigens can also induce numerous B—cells to activate; however, the immune response is weaker and the induction of memory is weaker than with T-helper cell activation. In contrast, activation of B—cells with T-helper cell activation results in a much better immune response and more effective memory.
This long-term, effective immune response is the type of reaction that is the goal of immunizations. This process then stimulates the B—cell s to mature into a plasma cell s which then begins production of the particular antibody with the best corresponding fit to the antigen. From these stimulated B-cells, clones of B-cells with the specificity for the particular antigen will arise.
These cells may become plasma cells producing antibodies or memory cells which will remain in the lymph nodes to stimulate a new immune response to that particular antigen. This occurs during the primary immune response when the immune system is first exposed to a particular antigen. This process of clonal selection and expansion will take several days to occur; and, primarily involves the production of IgM. IgM is the first antibody produced during a primary immune response.
As the immune response progresses, the activated plasma cells will begin producing IgG specific to the particular antigen. Although IgM is the first antibody produced and is a much larger antibody, IgG is a better neutralizing antibody.
IgG binds more effectively to the antigen and aids in opsonization. As a note, other antibodies can be produced by plasma cells. IgD is primarily found as a receptor bound to the surfaces of mature B—cells. While, IgA is the antibody found in secretions such as mucous, saliva, tears, and breast milk; and, IgE is the antibody involved in allergic reactions and parasitic infections.
However, the most important antibody for vaccines is IgG. With the memory cells that have been produced with the primary immune response, any succeeding exposures to the antigen will result in a more rapid and effective secondary immune response.
With this secondary immune response, the reaction will be quicker, larger, and primarily composed of IgG. As for the other arm of adaptive immunity, cell-mediated immunity, it functions primarily against intracellular pathogens. T-cells mature in the thymus and are then released into the bloodstream. CD4 cells are essential for antibody-mediated immunity and in helping B—cells control extracellular pathogens. There are two subsets of CD4 cells, Th1 and Th2.
Th1 cells help promote cell-mediated immunity; and, Th2 cells help promote antibody-mediated immunity. The MHC I protein is found on all nucleated body cells except for mature erythrocytes and acts as a marker of body cells.
CD8 cells are essential for cell-mediated immunity and in helping control of intracellular pathogens. Unlike B-cells, T-cells can only recognize antigen that has been processed and presented by antigen-presenting cells. There are two types of antigen processing. The first type of antigen processing involves attaching intracellular antigens along with MHC I proteins to the surface of antigen-processing cells.
This occurs with viral antigens and tumor cells. The other type of antigen processing involves attaching extracellular antigens along with MHC II proteins to the surface of antigen-presenting cells. This occurs with bacterial and parasitic antigens. Once the T-cell has been activated by the antigen-presenting cell, it begins to carry out its functions depending on whether it is a CD4 cell or a CD8 cell. As with B-cells, activated T-cells also undergo clonal expansion which produces additional effector T-cells for the current infection and memory T-cells for future infections with this antigen.
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