COVID-19 becomes a pandemic: how does this virus work to paralyze sufferers and prospects for drug trials?

ABEE MUSIC
0


 COVID-19 becomes a pandemic: how does this virus work to paralyze sufferers and prospects for drug trials?

Three of the 34 patients who tested positive for COVID-19, a respiratory disease caused by SARS-CoV-2 which is now a pandemic, in Indonesia are currently recovering and one has died.

 Globally, the latest data from the Corona Resource Center at Johns Hopkins University in the United States shows that of about 126,000 cases of COVID-19 worldwide as of March 12, 54% of them have recovered.  The mortality is around 3.6% (4,600 people).  This means that the number of patients who have recovered from COVID-19 is far more than those who cannot be saved.

 How can this virus kill such a small percentage of patients?  Also why did the majority of patients beat the virus and recover from the COVID-19 disease?  This is the explanation from the point of molecular biology.

 How the Coronavirus works

 Think of the virus as a terrorist who moves secretly to find the target's weak point.

He infiltrated the system of government of a country, hit its weak point, and at the right moment then paralyzed the country.  Then they build a stronger terrorist network to attack other countries.

 The body is also like a state.  The average human body is made of 30 trillion cells and contains 40 trillion bacteria.  The cells renew themselves continuously when something is damaged.  Cells have systems and powers to deal with their enemies, one of which is a virus.

 When not inside the host, a virus is really just a piece of genetic material (DNA or RNA) covered in protein.  Once this virus manages to infiltrate the cells of living things, whether animals, plants or humans, which then become the host, the virus can live and develop and then become an infectious agent that causes disease.

 SARS-CoV-2 was most likely transmitted from bats to humans.  Diseases caused by this virus are almost the same in the cases of SARS 2002 and MERS 2012. All three types of viruses can spread from human to human.

 Scientists are currently still researching how SARS-CoV-2 works.  However, based on its genome, the researchers saw that this virus appears to work in a way that is not much different from SARS-CoV, which caused the SARS outbreak in 2002 or other Coronavirus (CoV) groups.

 The International Virus Taxonomy Committee (ICTV) identified SARS-CoV-2 as a strain of SARS-CoV.  The virus that causes COVID-19 is the seventh virus from the CoV group that attacks humans after 229E, NL63, OC43, HKU1, MERS-CoV, and SARS-CoV.

 SARS-CoV-2 cannot reproduce without infecting the mammalian cell as its host or home.  This virus can infect cells in humans through matching receptors (protein molecules that receive chemical signals from outside the cell) on these cells.

 This virus has a surface receptor protein that can bind to an enzyme (ACE2) on the cell surface of the lungs (respiratory system) and small intestine (digestive system) by being triggered by certain enzymes on the host cell.  It is like a lock and key that fits, so it can cause an access opening.

 A recent study has shown that an enzyme in host cells, called furin, plays an important role in the bonding process between the SARS-CoV-2 virus and its host.  Furin is found in many tissues of the human body, including the lungs, liver, and small intestine.  Thus, the virus has the potential to attack many organs.

After binding to the host cell receptor, SARS-CoV-2 takes over the control machinery of the cell.  He then hijacked it to produce more genetic material for the virus as well as new individuals from the virus.  Then, the host cell will slowly die and be destroyed.

 This in turn can cause disruption at the tissue level to organ failure.

 Pulmonary attack phase

 Medically, the symptoms of COVID-19 can be seen from the onset of infections such as fever, cough, shortness of breath, and difficulty breathing.  However, some are actually infected but do not show any symptoms.

 The World Health Organization states that COVID-19 usually attacks the lungs in three phases: (1) viral replication, (2) immune system overreaction, and (3) lung damage.

 However, not all patients with this disease experience these three phases.

 In the initial conditions of infection, SARS-CoV-2 attacks human lung cells rapidly.  There are two types of cells that are attacked, namely cells that produce mucus (mucus) and cells with cilia (having a hair-like structure).

 SARS-CoV-2 infects and kills ciliary cells, which then slough off and fill the patient's airways with cell or tissue debris and fluid, thus preventing the organs from working optimally.

 In the next phase, the cells of the immune system begin to enter.  Our bodies fight disease by flooding the lungs with immune system cells to clear damage and repair lung tissue.

 But sometimes the immune system crashes and those cells kill anything, including healthy body tissue.  Even more debris clogs the lungs causing inflammation of the lungs (pneumonia) to get worse.

 Finally, lung damage continues to increase in the third phase.  This can lead to respiratory failure which can lead to death.

 Even if death does occur, some patients survive with very severe lung damage.  When that happens, the patient must be put on a ventilator to help his respiratory system until the patient's condition slowly improves and recovers.

 Meanwhile, inflammation in the lungs also makes the membrane between the air sacs and blood vessels more easily penetrated by a particle that can fill the lungs with fluid and affect its ability to meet the oxygen supply in the blood.

 Data from 44,000 COVID-19 patients, according to the World Health Organization, 81% experienced mild symptoms, 14% severe symptoms, 5% seriously ill, between 1% and 2% died from the disease.  In addition, the patient's incubation period was initially set at 1-14 days.  Now, the incubation period has been increased to 28 days.

 Drug trial

 Although there is currently no cure for COVID-19, a number of researchers have been and are currently testing drugs that were previously used to disable other viruses.  A number of drugs show positive results.

 For example, a group of researchers from Imperial College London concluded that baricitinib (an arthritis drug) was effective at reducing the ability of the SARS-CoV-2 virus to infect lung cells.  This research is computer modeling (in silico), that is, using certain software we can predict interactions between drug candidates and viruses whose genomes have been mapped.

 Baricitinib can interfere with the mechanism of viral entry into host cells.  This drug is also able to block the pathway of proteins in cell signaling pathways that have the potential to increase inflammation or inflammation in tissues or organs.

 A team at the Chinese Academy of Sciences and the Beijing Institute of Pharmacology and Toxicology who tested it on a laboratory scale (in vitro) found that remdesivir and choloroquine (an antimalarial and autoimmune disease drug) were effective enough to attenuate SARS-CoV-2 infection.

 Remdesivir has been recognized as a promising drug against SARS/MERS-CoV and Ebola virus infections.  Tests on cultured cells, several experimental animals, and non-human primates against previously emerged viruses have been carried out.  Remdesivir is known to work by stopping the maturation of the virus in host cells that have been infected with the virus.

 Chloroquine is known to inhibit viral infections by increasing the degree of acidity in cells required for virus or cell fusion, and by interfering with viral receptors.  Chloroquine also stimulates immune enhancement which synergistically enhances its antiviral effect.  The drug is widely distributed throughout the body after oral administration, including in the lungs.

 To date, chloroquine is a cheap and safe drug that has been used for more than 70 years and has clinical potential to fight SARS-CoV-2.

 Actually, COVID-19 patients can recover without medication as long as the patient's immune system is strong and improved.  The majority of those who died, according to a research based on patient data in China , were elderly patients whose immune systems were weak and suffered from several complications before being infected with this virus, such as diabetes, hypertension, and heart disease.

Post a Comment

0Comments

Please Select Embedded Mode To show the Comment System.*