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STUDENT'S MAGAZINE \



           Fortunately, around 80% of patients experience mild or no symptoms (Business Insider). WHO’s
           recommendations are to stay home and adopt healthful behaviors, especially washing your hands
           frequently, covering your nose and mouth when you cough or sneeze, and maintaining social dis-
           tance inside and outside the home. Infected individuals should also wear face masks to avoid spread-
           ing the disease. For this group, medical intervention is unnecessary as they can gradually recover,
           letting their immune systems do the work. Early symptoms may be relieved by taking painkillers
           such as paracetamol/Tylenol (National Health Service).

           The rest comprise severe (15%) and critical (5%) cases, which require hospitalization (Worldome-
           ter). The elderly, as well as people with chronic health conditions like heart disease, diabetes, and
           high blood pressure, are most at risk for major complications involving COVID-19. Generally, the
           coronavirus resides in the upper respiratory tract, primarily the nose and throat, but it sometimes
           makes its way down. The real trouble begins once it infects the lungs—this is when the virus “kills”.
           Patients are likely to develop fluid in their alveoli—air sacs in the lungs—leading to pneumonia and
           shortness of breath. Respiratory failure, multi-organ failure, and death may follow if the severity
           intensifies. Oxygen delivery is needed to mitigate breathing difficulties; it comes in various forms,
           including supplemental oxygen via a nasal mask, mechanical ventilation, and extracorporeal mem-
           brane oxygenation (ECMO)2.


           The Corona Factory
           A virus operates by invading a person’s host cells and then hijacking the cellular machinery, or
           organelles, to produce more copies of itself. Each virus strain has a different mechanism. Here’s a
           rundown of what SARS-CoV-2 does to our cells:
           Spike protein on the virus binds to cell surface receptors (ACE2), granting access to the cell. These
           receptors are abundant in the respiratory tract.
           Once inside, it releases and uses its genome3 (RNA) to make polyproteins, which are broken down
           into non-structural proteins, forming a replicase-transcriptase complex4.
           With the help of the complex, the genomic RNAs are replicated, some of which will end up as the
           new virion’s genome.
           The complex turns other replicated RNAs into structural and accessory proteins.
           The Golgi apparatus, an organelle, assembles and packages everything (genome, proteins, and other
           materials) together to create virions.
           Mature virions are released out of the host cells, which are damaged or destroyed in the process.
           The viruses attack more cells, replicating into more copies.
           Our immune system kicks in and fights off these invaders. In severe and critical cases, the immune
           response goes into overdrive, unleashing cytokine storms5 that further injure the respiratory tree
           and cause inflammation.

           Counterattack I: Medications
           If we can prevent or disrupt any step of the viral replication cycle, then an infected individual will
           soon get better—this is the rationale behind antiviral drugs. Antivirals target and disable particular
           viral proteins or parts of proteins which are unlike the ones found in humans to circumvent unin-
           tentional cellular damage.

           There’s yet to be a definitive medicine for COVID-19. Researchers are now repurposing existing
           drugs to see if they benefit patients suffering from this emerging disease. Since these drugs are al-
           ready FDA-approved and have safely been utilized for other viral diseases, it’s simpler to test them
           than to develop a brand-new one, which often takes years of research. Pharmaceutical firms hope
           that in their massive database of drugs, there will be at least one that does the job.


           A few drugs directly attack the virus, attempting to halt its replication. An investigational intrave-
           nous antiviral, remdesivir was intended to be used against Ebola and Marburg viruses. Although
           its original objective wasn’t a success, it has recently been in the limelight as the “most promising
           COVID-19 drug” (Drug Target Review). It inhibits the production of the RNA-dependent RNA

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