This Is How Your Immune System Responds to COVID-19 And Distribution of Its Functional Receptor

Most of the people get infected with novel coronavirus can have reportedly various results. This whole reaction depends on the immunity of the infected person. Likewise, some people can report nothing more than symptoms of mild cold; whereas many others are hospitalized and even lacking of good immunity boosting power, people die as their lungs become inflamed and fill up with fluid. Here, a simple question arises is; How can the same virus result in such different results ?

Scientists all over the world are still confused of this action by Coronavirus. But here we all are

getting the idea for crucial role of immune system of person coming in contact with it.

Here it depends, whether the person who is getting infected will die of it or will recover from

it.

" In fact, most of the cases

being reported world-wide, so,

outcomes of this, depends on

the functioning of immune system

of the person being infected, whether

Person will die or will recover."

The standard immune procedure for encountering the virus, your body launches its standard innate immune defense. This process involves the release of proteins called Interferons that interfere with virus's ability to replicate inside the body's cells. Simultaneously, Interferons recruits other

immune cells, like, Cytotoxic T cells, Natural Killer(NK) cells, and Antiviral Macrophages, these cells have the ability to recognize and kill the virus-infected cells. Humoral immunity also plays an important role in viral infection, virus-infected cells can stimulate B lymphocyte to produce specific antibody for the virus. Antibody neutralization is more effective when virus is present in large fluid spaces(e.g., serum) or on moist surfaces(e.g., Gastrointestinal tract and Respiratory tract). IgG, IgM, and IgA have all been shown to exert antiviral activity. Antibody can neutralize virus by: 1) blocking virus-host cell interactions or 2) recognizing viral antigens on virus-infected cells which can lead to antibody-dependent cytotoxic cells (ADCC) or complement-mediated lysis. IgG antibodies are responsible for most antiviral activity in serum, while IgA is the most important antibody when

viruses infect mucosal surfaces. The activation of different immune functions and the duration and magnitude of the immune response depend on how the virus interacts with host cells (on whether it is a cytolytic, steady-state, latent, and/or integrated infection) and on how the virus spreads (by local, primary hematogenous, secondary hematogenous, and/or nervous system spread).

On the basis of viral antigen interaction with host cells (depends on the immune system of person, which usually weakens as age increases), the period in which virus establishes itself, and where in the body virus takes hold, symptoms of persons are devised, whether it can be mild symptoms or severe symptoms.

The novel coronavirus gains entry into a cell by locking onto a specific protein ACE-2(metallopeptidase-Angiotensin Converting Enzyme-2) receptor that sits on the cell's surface.

Although ACE-2 mRNA is known to be present in virtually all organs, its protein expression is largely unknown. Since identifying the possible route of infection has major implications for understanding the pathogenesis and future treatment strategies for SARS, recent study reveals the localization of ACE-2 protein in various human organs (oral and nasal mucosa, naso-pharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain). The most remarkable finding was the surface expression of ACE-2 protein on lung alveolar epithelial cells and enterocytes of the small intestine. Furthermore, ACE-2 was present in arterial and venous endothelial cells and arterial smooth muscle cells in all organs.

ACE-2 receptors are mostly abundant in lungs, secondly in intestine, which could explain why many people with novel coronavirus experience respiratory illness and diarrhea respectively. A distinct coronavirus also has been identified as aetiological agent of  SARS - Severe Acute Respiratory Syndrome, that's why SARS-CoV.

Because, the mode of transmission through droplets, if it comes to your mouth and enters your oropharynx, then it has two options where it can reside from there. It can transit into the lung through trachea from the oropharynx during breathe in process or due to swallow reflex, secondly it can go down to your intestine through stomach.

In some people, however, the virus will replicate and spread rapidly before the immune system start its function to control it. By the two reasons this can happen are if a high quantity of viral particles infect the body - which is why doctors and nurses, who are exposed huge amounts of virus multiple times a day caring for patients, can have more severe infections even if they are healthy and young. The more the quantity of virus inside the body, harder it will be for immune system to manage it.

Another, important reason the body can lose control over the corona virus lies in the immune system itself. Susceptibility of the population during this pandemic are elderly people, whose immune system naturally start to decline with age, and people who is immunosuppressed because of another illness or medication. A weaker immune system will result in weaker initial Interferon response or a delayed antibody response, allowing the virus to spread from cell to cell relatively unchecked. If the Antibody Neutralization is good, then there are chances of recovery is more. If virus is able to hold in lungs, it can lead to many lungs related problems, like, pneumonia as more cells become infected and inflamed. There is really great curiosity for this CoViD-19. For now, your best companion to counter this coronavirus is to support your immune system with sleep, exercise, and good nutrition and, most importantly to wash your hands and practice social distancing so you don't get infected.
For more information on Novel Corona Virus COVID-19, please visit
cdc.gov
References :- J Pathol. 2004 Jun;203(2):631-7,

Department of Pathology and Laboratory Medicine, University Hospital Groningen, The Netherlands
2) Gary R. Klimpel. Chapter 50: Immune Defenses, Medical Microbiology 4th edition by Baron S.