5 tips on how to Overcome Coronavirus (COVID-19) in June 2020

    Coronavirus (COVID-19) Overview

    Coronavirus is a family of viruses that can cause respiratory infection. The illness caused by coronaviruses in humans can range from the mild common cold to more severe diseases like COVID-19, which can be fatal. Common human coronaviruses are contagious and are easily spread from person to person. They are spread through close contact with someone who is infected via secretions from coughing and sneezing or touching objects that have the virus on them. 

    Coronavirus (COVID-19)
    Coronavirus (COVID-19)

    Symptoms of Coronavirus

    Symptoms of coronavirus illness vary depending on the specific virus. For the milder strains, respiratory symptoms like a runny nose, headache, cough, sore throat, fever, and fatigue are common. If the infection progresses to something more severe, it can cause pneumonia, bronchitis, organ failure, and even death. It is more likely to happen in children, the elderly, and people with weakened immune systems.

    1.Coronavirus damage on respiratory tract

    Covid-19 affects the respiratory tract in humans. The infection starts with mild flu-like symptoms or no symptoms and further progress to severe symptoms. COVID-19 primarily infects the lungs in the affected individuals and, in severe cases, causes death due to ARDS and pneumonia. It is important to remember that it does not lead to ARDS and pneumonia in all the cases, which is an occurrence in most severe cases.
    In the majority of the cases, i.e., 80% will exhibit mild symptoms, 14% will have pneumonia, 5% will suffer from septic shock, and organ failure (mostly respiratory failure), and in 2% cases, it will be fatal.

    2.Acute Respiratory Distress Syndrome (ARDS)

    There is a direct correlation between Covid-19 and ARDS. Severe cases of Covid-19 infection lead to ARDS and pneumonia, which can prove to be fatal for the infected individual.
     Acute Respiratory Distress Syndrome causes dry cough, heavy breathing, breathing difficulties, and increased heart rate. In most healthy individuals who do not have underlying issues, COVID 19 exhibits mild symptoms, which can be treated with medications, and eventually, the patients recover. 
    In severe cases, where the infected person has an impaired immunity due to underlying health conditions, an infection due to COVID 19 can progress to severe ARDS. Once the patient progresses to ARDS, it eventually leads to pneumonia.

    Effect of ARDS on the lungs

    COVID 19 directly impacts the lungs and damages the alveoli (tiny air sacs). The function of the alveolus is to transfer oxygen to the blood vessels. These blood vessels or capillaries carry the oxygen to the RBCs (Red blood cells). 
    It is the RBCs that finally deliver the oxygen to all the internal organs in the body. 
    The virus works by damaging the wall and the lining of the alveolus and capillaries. The debris from the damage, which is a plasma protein, accumulates on the alveolus wall and thickens the lining. As the walls thicken, the transfer of oxygen to the red blood cells is impaired. The thicker the wall gets, the more difficult it gets to transfer oxygen to the red blood cells, which causes difficulty in breathing as the body is running short of oxygen. 
     The lack of oxygen in the internal organs results in a deficiency in the body and diminish the functioning of the organs. 
    At this juncture, the body fights to increase oxygen intake.
    And the first response of the body is to destroy the virus and prevent its replication, but if the individual has weaker immunity, then the body is unable to stop the virus.


    As the air sacs are damaged, there is an influx of liquid, which is mostly inflamed cells and protein, and this fluid build-up leads to pneumonia.it is further impairs the oxygen intake by the lungs and hinders the oxygen exchange. Due to the novelty of the COVID 19 strain, there is no immediate treatment to cure pneumonia in COVID-19 patients directly and are mostly given supportive care.

    Mode of action of COVID-19 on the lungs

    Replication cycle


    Infection begins when the viral spike protein attaches to its complementary host cell receptor. After attachment, a protease of the host cell cleaves and activates the receptor-attached spike protein. Depending on the host cell protease available, cleavage and activation allow the virus to enter the host cell by endocytosis or direct fusion of the viral envelope with the host membrane. 


    On entry into the host cell, the virus particle is uncoated, and its genome enters the cell cytoplasm. The coronavirus RNA genome has a 5′ methylated cap and a 3′ polyadenylated tail, which allows the RNA to attach to the host cell's ribosome for translation. The host ribosome translates the initial overlapping open reading frames ORF1a and ORF1b of the virus genome into two large overlapping polyproteins, pp1a and pp1ab.  
    The polyproteins have their proteases, PLpro and 3CLpro, which cleave the polyproteins at different specific sites. The cleavage of polyprotein pp1ab yields 16 nonstructural proteins (nsp1 to nsp16). Product proteins include various replication proteins such as RNA-dependent RNA polymerase (RdRp), RNA helicase, and exoribonuclease.

    Replicase-transcriptase complex

    A number of the nonstructural proteins coalesce to form a multi-protein replicase-transcriptase complex (RTC). The main replicase-transcriptase protein is the RNA-dependent RNA polymerase. It is directly involved in the replication and transcription of RNA from an RNA strand—the other nonstructural proteins in the complex assist in the replication and transcription process.


    One of the main functions of the complex is to replicate the viral genome. RdRp directly mediates the synthesis of negative-sense genomic RNA from the positive sense genomic RNA. This is followed by the replication of positive-sense genomic RNA from the negative-sense genomic RNA.

    Transcription –

    The other important function of the complex is to transcribe the viral genome. RdRp directly mediates the synthesis of negative-sense subgenomic RNA molecules from the positive-sense genomic RNA. This process is followed by the transcription of these negative-sense subgenomic RNA molecules to their corresponding positive-sense mRNAs.


    The replicase-transcriptase complex is also capable of genetic recombination when at least two viral genomes are present in the same infected cell. 

    RNA recombination appears to be a significant driving force in determining genetic variability within a coronavirus species, the capability of a coronavirus species to jump from one host to another and, in determining the emergence of novel coronaviruses. The exact mechanism of recombination in coronaviruses is unclear but likely involves template switching during genome replication.



    The mRNAs are gene transcripts of the last third of the virus genome after the initial overlapping reading frame. 

    These mRNAs are translated by the host's ribosomes into the structural proteins and several accessory proteins. RNA translation occurs inside the endoplasmic reticulum. 

    The viral structural proteins S, E, & M move along the secretory pathway into the Golgi intermediate compartment.

     There, the M proteins direct most protein-protein interactions required for the assembly of viruses following its binding to the nucleocapsid.

     Progeny viruses are then released from the host cell by exocytosis through secretory vesicles. Once released, the viruses can infect another host


    Effect of COVID-19 on entire body:


    Whether the new coronavirus SARS-CoV-2 itself causes this damage to the heart or as seems more likely, the harm is done by the immune reactions triggered by the infection that remains to be seen. However, acute heart damage has also occurred in the past in some SARS and MERS patients, and these SARS-CoV and MERS-CoV pathogens are very closely related to the current coronavirus SARS-CoV-2.


    During the COVID-19 disease, the lung is massively attacked; it is harder for oxygen to reach the blood vessels, stiffens the lungs, and makes breathing shallow and rapid. Respiratory disorders, shortness of breath and a dry, irritable cough are the consequences; physical performance decreases, and even everyday activities become difficult. Pulmonary fibrosis cannot be cured because the scarred changes in the lung tissue do not regress. But the progression of the condition can be delayed and sometimes even stopped if it is detected in time.


    The researchers concluded that the novel coronavirus SARS-CoV-2 leads to a generalized inflammation in the endothelium via ACE2 receptors. This could lead to severe microcirculatory disturbances that damage the heart and cause pulmonary embolism and a vascular occlusion in the brain and intestinal tract. As a result, multiorgan failure occurs, which can often lead to death.


    If COVID-19 patients with pneumonia need to be ventilated, this can also damage the kidneys. Acute kidney failure often occurs. Because pneumonia often causes a lot of fluid to accumulate in the lungs, patients are given a drug that removes fluid from the body. However, this reduces the blood supply to the kidneys, and they can no longer fulfill their cleansing function.
    In addition, the blood coagulates faster in severe COVID-19 disease. As a result, blood clots can easily form, blocking the blood vessels and often also the kidneys. Small infarctions in the kidney tissue have been observed in numerous patients.


    The novel coronavirus SARS CoV-2 also appears to cause visible damage to the largest organ of the human body, the skin.

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