Innate versus Adaptive Immunity in COVID-19

By | November 6, 2021

The 2019 Corona virus epidemic (COVID-19) has affected millions of people worldwide, with more than 4.5 million deaths. The most surprising aspect of this epidemic is that most of the infected people have no mild or severe symptoms and a significant minority causes serious or serious illness.

Numerous studies have investigated the immunological effects of Corona virus 2 (SARS-CoV-2), an acute acute respiratory syndrome, and have sought to determine the severity and risk factors for the disease. They are congenital and provide information about the adaptive immune response.


Immunity against the virus

Cytokines are cellular signaling molecules involved in many biological and immunological activities. One of them is congenital and adaptive immune-mediated pleotropic cytokine interleukin-6 (IL-6). It helps regulate the differentiation of immune cells, as well as warns against rogue attacks and ischemic damage.

IL-6 also mediates plasma cell growth and the formation of immunoglobulin antibodies. High levels of IL-6 expression in autoimmune disorders also play a role in these conditions. Similarly, in COVID-19, the IL-6 virus appears at a higher level after entering the lung epithelium.

SARS-CoV-2 stimulates alveolar and circulating macrophages, resulting in cytokine storms caused by excess moisture in IL-6. It causes damage and damage to endothelial cells, the fluid and secretions of capillaries and alveoli that can pass. Acid Respiratory Syndrome (ARDS) is an important procedure.

He suggested the use of IL-6 receptor inhibitory monoclonal antibody tocilizomab to modulate the severity of ARDS.

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Many of the symptoms of severe COVID-19 pneumonia can be caused by systemic over-activation. These include ARDS and hypercoagulation. In these pneumonia patients, high levels of IL-6 stimulate appendages through the C5a-C5a receptor (C5aR) axis.

What is collective exemption?

In addition to the severity of the symptoms, all signs of inflammation gradually increase from asymptomatic to critical COVID-19. Classical and alternative pathways may be more closely related to the phenotype with the participation of multiple activation pathways. These pathways are activated by the immune complex of the IgG virus.

C5a / C5aR1 axis blockage can prevent the development of signs of inflammation and lung injury in these patients. In addition, patients with CoVID-19 pneumonia often develop adverse events due to the strong functioning of the adrenal system. This can be prevented by blocking additional activation.

Another way to increase activation may be to develop ARDS in patients infected with the virus. Here, the C1 esterase inhibitor (C1-INH) works in a number of ways to regulate the intracellular pathway. Patients with COVID-19 pneumonia may be helpful in treating the pathway between the congenital immune system and the clot.

Adaptive Immunity – Antibodies

This signature of the immune response is related to the mediated effects of B and T cell viruses. The initial antibody response involves IgM and IgA, with more IgG being released within 10 days. This immune response protects against viral infections and provides high levels of IgG memory B cells.
Antibodies (RBDs) against receptor binding sites are important predictors of antiviral protection. Effective antibodies to prevent infectious diseases are those that target RBD and associate it with the highest trimmer.

First, follicular T cells activate simple B cells that grow into active B cells. They make B cells, IgG or plasma producing cells. These changes occur in the bacterial centers of the follicles. There is a short lifespan that inhibits this phase of the antibody effect of plasma plastids. Subsequent creation stimulates memory B cells and long-term plasma cells in the bone marrow and triggers an antibody response against RBD.

T-cell memory retains the ability to respond to virus antigens, resulting in direct cytotoxic activity to clear T-cell viruses and enhance the response of B cells.

However, antibody titers vary from person to person and the highest levels are between 50 and 60 days. They can stay on the protection level for 10 months. Too much IgG antibody response to the virus can lead to systemic inflammation, multiple organ failure, and even the release of heavy cytokines that can lead to death.

Adaptive immune system – T cells

Acute CD4 T cells are present in the blood of more than 80% of people infected with SARS-CoV-2, as well as in more than one in three healthy donors. Otherwise, these cells respond to epitopes in the C-terminal domain of the fibrous protein. These cells also bind to several proteins of the human native corona virus 229E and OC43.
This may mean that the reactive T cells found in these donors were due to a previous seasonal corona virus infection. However, they may explain that children and young adults are less likely to have symptomatic infections. This discovery neutralizes antibodies against the human corona virus, which is high for early strains. Thus, CD4 T cells are the key to effective and permanent resistance to human coronavirus infection, including SARS-CoV-2.

Most COVID-19 patients have an interferon alpha (IFN-α) reaction. Patients with moderate symptoms and successful recovery show a variety of CD4 and CD8-affecting T cells and natural killer cells, which then interact with FcγR IIIb receptors.

It responds to a number of viral proteins,

Such as T cells, as well as membrane (M) and nucleoprotein (N) antigens, and reaches the highest levels in about one-third and one-half of patients. Not only does this indicate a protective immune profile, but future vaccines may contain more than one protein, a single immunodeficiency T cell reactive peptide.

In contrast, acute illness was associated with exceptionally strong and permanent immunity. Prolonged release of IFN-led to a decrease in T cells and abnormal accumulation of T cell receptors, as well as the proliferation of T cells without NK cell activation. Second, antibody-dependent cellular cytotoxicity (ADCC) is an important symptom of virulence.
The rapid increase in the number of cells secreting IFN-ing in patients with COVID-19 pneumonia suggests that this treatment should be stopped.

Patients with the highest levels of the disease have the highest CD4 and CD8 T-cell responses to various SARS-CoV-2 antigens. However, central memory and infectious CD8 T cells are determine to be anti-protein in COD-19 patients. These are each other’s reactions, indicating the presence of long-term immunity.

These cells may be present in the airways to enhance the immune response to the rapidly growing new SARS-CoV-2 virus. Although the production of antibodies, along with T cells, can provide rapid bactericidal immunity when the antigen is detected, the antigen must appear and activate the memory response to initiate the process of virus eradication. Should. This also means that not only is there a change in the phenotype of the disease that may occur, but also that people without a symptomatic infection can carry and infect the virus as long as they have a cellular and comorbid response. Don’t get rid of it.

People without exception

Scientists have found a link between human leukocyte antigen (HLA) DQB1 * 06 and the risk of a serious disease. This can help determine if there are people who can’t resist the virus, but who aren’t immune to superheroes. Immunity against viruses and vaccines.

In people without immunity, such as those receiving chemotherapy or immunosuppressive drugs, the virus can last up to two months after infection. Despite the development of persistently viral spread antibodies in a quarter of kidney transplants that lasted at least two months. The presence of viral particles in the blood indicates a low probability.

Defensive time

Adaptations in the patient’s sample show that the true measure of the immune response was found five months after infection with infect IgG and anti-RBDIG. However, no smooth curve was obtain indicating that the response to SARS-CoV-2 was different.

It should be note that the reaction of memory B cells and T cells of central memory continues and the infection increases up to five months. If confirm, it means that the virus is very long and has a specific B cell and IgG response. Some viruses, such as the 1918 H1N1 influenza virus and the 60-year-old bottle vaccine, cause B-memory cells 90 years after infection.

New treatments need to be develop base on these findings to control the epidemic. Such research is the best way to understand SARS-CoV-2 immunology and develop a better vaccine.

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