The Novel Coronavirus, commonly known as the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2 ), is a zoonotic agent that causes the Coronavirus Disease 2019 (COVID-19).¹ A group of Rhinolophus bats are said to be the source of it, and it is supposed to have started in the city of Wuhan, People’s Republic of China.² Since then, it has quickly spread around the globe, largely through personal contact and respiratory transmission. Clinical signs and symptoms of coronavirus disease included elevated body temperature, cough, headache, nausea, vomiting, anorexia, diarrhea, dyspnea and numerous organ dysfunctions. Many infected people, experienced only minor illness symptoms and recovered. Some patients experienced a progression of major side effects, such as sepsis, acute respiratory failure, metabolic acidosis, heart failure, renal injury and hypoxic encephalopathy, before passing away from their disease.^3–5 The patients in other asymptomatic cases, on the other hand, did not display any acute COVID-19 symptoms. They occasionally also have a slight fever, little to no exhaustion and no respiratory issues. These asymptomatic patients may, however, be SARS-CoV-2 carriers who spread the virus to other people’s bodies.⁵ Acute Respiratory Distress Syndrome (ARDS), immunological derangement, coagulopathy, septic shock and Multiple Organ Dysfunction Syndrome (MODS) are possible progressions in severe patients.⁶ In order to raise general awareness among the public, an effort was made to highlight the molecular and biochemical changes that occur during COVID along with its management by treatment with drugs, drug delivery system, immune booster and breathing exercises or yoga.

During COVID-19 various biological changes in some of systems or systemic conditions of body were observed as given below:

Cardiomyocyte damage, both direct and indirect, is a common symptom of COVID-19 infection. There are various types of injuries that can result in these conditions, including acute myocardial infarctions, heart failure, myocarditis, arrhythmias, cardiac arrests, sepsis, septic shock, and pulmonary emboli.

However, the mechanisms underlying the phenomenon remain unresolved, a few hypotheses have emerged, including cardiac stress caused by hypoxia and respiratory failure, direct SARS-CoV-2 infection of ACE2 receptor-expressing myocardial cells and indirect changes brought on by systemic inflammatory response.⁷ Therefore, the early detection of heart injury and quick intervention may be advanced through the measurement of cardiac damage biomarkers throughout the hospital stay in COVID-19 patients.⁸ An injury to the heart was also caused by the advancement of atherosclerosis and increased plaque rupture vulnerability.⁹ Additionally, cytokine storm and high intracellular calcium caused by hypoxia are alternative pathways that result in cardiac myocyte death.¹⁰

Segment Elevation Myocardial Infarction (STEMI) and magnified acute CV events^11–13 are associated to air pollution exposure and COVID-19 infection, respectively.^14,15

Psychiatric and neurological disorders may raise the likelihood of acquiring COVID-19.^16–18 The risk of Alzheimer’s disease is increased by one of the most significant factors of cognitive impairment, social exclusion as a result of isolation.¹⁸ Delirium was a severe COVID-19 presentation in elderly people with a history of neuropsychiatric illness. These people thereafter showed signs of motor and cognitive abnormalities, including agitation, stiffness, abulia and alogia. C-Reactive Protein (CRP) levels in the blood also increased along with neurological and cognitive abnormalities.^19,20

Acute inflammation caused by pneumonia, along with COVID-19 drug toxicity, have resulted in liver damage in patients with COVID-19. Examples of direct liver assault include the effects of coagulopathy and endothelial aggressiveness in tiny intrahepatic arteries, as well as the direct cytopathogenic effects of SARS-CoV-2 on hepatocytes and cholangiocytes. Less than 10% of patients had significant liver damage (ALT more than 5 times higher than the usual value), while the majority of patients with abnormal AST/ALT readings exhibited a moderate rise between 1-2 times than normal values. Injuries to the liver were mild in 30% of individuals (between 2 and 5 times higher than the normal value).^21,22

Hypertension and Type 2 Diabetes Mellitus (TDM2) are common conditions in COVID-19 patients. In roughly 10% of TDM2/ COVID-19 patients, a SARS-CoV-2 infection may cause the production of hyperglycemic hormones (such glucocorticoids and catecholamines) as well as bouts of hypoglycemia (with increased pro-inflammatory monocytes and platelet reactivity).^13–15 Although there was no statistically significant difference in CRP or Troponin-I levels, in COVID-19 positive patients with or without diabetes tended to have greater levels of both. There is a possibility that this pattern indicates a higher risk of cardiac failure in patients with COVID-19.¹⁶

SARS-CoV-2 uses the Angiotensin-Converting Enzyme 2 (ACE-2) receptors on human cells, including endothelial cells, as part of an unusual mode of infection.²³ Clotting activation, which is commonly reported in patients with COVID-19,^24,25 is caused by binding to ACE-2 receptors on endothelial cells. These receptors induce localized inflammation, endothelial activation, tissue lesions and changes in cytokine release (Tumor Necrosis Factor [TNF]-, Interleukines [IL-1, IL-2 and IL-6]). In between 70 and 95% of individuals with severe COVID-19, there were several coagulation abnormalities observed, the most important of which included a moderate thrombocytopenia. Patients with and without COVID-19, there was no change in mortality with heparin use.²⁶

Comparing pregnant COVID-positive women to COVIDpositive non-pregnant women, the likelihood of ICU admission is greater in the former group. The risk of haematological issues was higher in pregnant women with COVID-19 (16%) compared to pregnant women without COVID-19 (0%).²⁷

The above effects in different important systems of body during COVID-19 lead to variations in the levels of different biochemical parameters as shown in Table 1.

Patients who have recovered from COVID-19 may nevertheless endure long-term symptoms due to changes in gene expression brought on by the new coronavirus.⁴³ Individual vulnerability, severity, and consequences of COVID-19 can be explained in part by host genetic variables such as variations in the ACE, ACE2, TMPRSS2, TMPRSS2A, HLA genotype and ABO blood group.⁴⁴

A genetically susceptible site has been discovered in severe COVID-19 patients with respiratory failure that is part of the 3p 21.31 gene cluster, which includes the genes SLC6A20, LZTFL1, FYCO1, CXCR6, XCR1 and CCR9.^45,46 Additionally, it has been discovered that low CXCR6 expression and elevated SLC6A20 expression in the population are dangerous.⁴⁷ HLA-B, an allele of the HLA genetic system, is susceptible to COVID-19 according to a different study.⁴⁸ Predicting strong binders across certain HLA alleles can make a contribution to development of an efficient COVID-19 vaccination with the proper epitope targets since COVID-19 vaccines may have a wide range of binding affinities with different HLA genotypes in different populations.⁴⁹ The SARS-VoV-2 susceptibility and post-infection survival may be correlated with ABO blood types. Blood type “O” is slightly protective, but blood type “A” is associated with a greater incidence of COVID-19.^50,51 A 1-base pair (bp) insertion in the DPP7 transcription may have a monogenic effect for COVID-19 patients who are asymptomatic.⁴⁷ The IFITM3 gene’s rs12252 C-allele homozygosity and the severity of the COVID-19 illness are associated, and individuals who are CC-homozygote have a 6.37-fold higher risk of developing the disease.⁵² Correlations between the COVID-19 variable recovery and prevalence rates and the ratio of the ACE 1/D allele frequency and regional variations of the ACE 1/D variant have been found.^53–56

After confirmation of diagnosis of COVID disease and observation of results of different biochemical tests the treatment is followed with a definite protocol. The treatment protocol consisted of following class of drugs.

Against RNA viruses such as Coronaviruses and Flavisviridae, Remdesivir is a potent inhibitor of RNA polymerase. It is a monophosphate prodrug that metabolises to an active C-adenosine nucleoside triphosphate analogue.⁵⁷ With EC₅₀ and EC₉₀ values of 0.77 and 1.76 M, it has exceptional in vitro activity against several coronaviruses, including SARSCoV2. It was believed that COVID-19 might be treated when it initially started to spread.^58,59 Remdesivir is being tested with a single 200 mg loading dosage and a daily 100 mg infusion. However, treatment with remdesivir is not advised for those whose estimated glomerular filtration rate is less than 30 mL/min.⁶⁰ Reactions at the infusion site, gastrointestinal dysfunction, and hepatic malfunction (elevated transaminase levels) have all been connected to Remdesivir therapy’s side effects.⁶¹

Favipiravir is a pyrazine carboxamide derivative that has been shown to be an effective against coronavirus, bunyavirus, flavivirus, filoviruses, and the Ebola virus.⁶² This prodrug suppresses RdR and is proven to inhibit SARS-CoV-2 (EC₅₀ = 61.88 M: CC₅₀ = over 400 M).⁶³ This treatment helped to decrease the SARS-CoV-2 presence in nasal secretions.⁶⁴ In a study, FPV also demonstrated the control of inflammatory mediator and pneumonia advancement in COVID^65,66 with improved lung histology.^67–69

It is a legitimate anti-malarial medication that is also used to treat autoimmune diseases. In an in vitro study, chloroquine was shown to be highly effective in preventing SARS-CoV-2 infection in host cells at the entry and exit stages.⁶⁸ However, the current use of these drugs to combat COVID-19 has recently been considered risky due to adverse events such as life-threatening arrhythmias, drug rash and hepatitis. Azithromycin (500 mg daily for 5 days) and Hydroxychloroquine (400 mg twice on day 1 and 200 mg twice daily for 5 days) showed QTc prolongation, which may instigate arrhythmia and sudden cardiac death, in COVID-19, as determined by the results of the experiment.⁶⁹Since it prolongs the QT interval, hydroxychloroquine should be used with caution, especially in those with co-morbidities and those who take such medications.⁷⁰

In order to be successful against SARS-CoV, LPV/RTV, the approved anti-HIV medications that specifically target the HIV protease⁷¹ and are anticipated to act on the viral 3-chymotrypsin- like protease.⁷² When LPV/RTV treatment is started within 10 days of the beginning of symptoms, virus shedding was dramatically reduced⁷³ and when combined with IFN- or RBV, COVID-19 patients’ health was improved with lower mortality rates.^74,75

NS5A and NS5B polymerase inhibition is the mechanism through which the antiviral drugs sofosbuvir and daclatasvir to prevent viral RNA replication.^76,77 Since SARS-CoV-2 shares RNA replication processes with other RNA viruses, it may be possible for Sofosbuvir and Daclatasvir to effectively block SARS-CoV-2 replication when used together.^78,79

Nirmatrelvir, an orally accessible protease inhibitor, is effective against MPRO, a viral protease that cleaves the two viral polyproteins and is crucial for viral replication,⁸⁰ also proven to be antiviral against all coronaviruses.⁸¹ Ritonavir co-administration raised the Nirmatrelvir concentrations to the desired therapeutic range The COVID-19 treatment Guidelines Panel (the Panel) suggests using Nirmatrelvir 300 mg with Ritonavir 100 mg (Paxlovid) orally twice daily for 5 days in non-hospitalized patients with mild to moderate COVID-19 aged 12 years and weighing 40 kg who are at high risk of disease progression. Patients who have hepatitis, abnormal liver enzyme tests, or pre-existing liver problems should use this medication with care.⁸²

Due to Molnupiravir’s potent antiviral activity against SARS-CoV-2, the FDA has given an Emergency Use Authorization (EUA) for its use in the treatment of mild to moderate COVID-19. This is because Molnupiravir is an oral prodrug of beta-D-N4-hydroxycytidine (NHC), which has a significant antiviral effect.^83,84 Molnupiravir has a low risk for genotoxicity, according to FDA’s assessment of the data on genotoxicity that are currently available.⁸⁵ Concerns have also been raised about Molnupiravir’s potential impact on the frequency of SARS-CoV-2 mutations. Molnupiravir has been linked to foetal harm in animal studies.

A family of cytokines called interferons have antiviral effects both in vivo and in vitro. The Food and Drug Administration (FDA) has approved the interferon beta-1a for the treatment of COVID-19 and relapsing types of multiple sclerosis. The COVID-19 Treatment Guidelines Panel (the Panel) does not recommend systemic interferon beta for the treatment of COVID-19 hospital patients (AI). The Panel advises against treating hospitalised COVID-19 patients with interferon alfa or lambda outside of a research study (AIIa).⁸⁶

The Food and Drug Administration (FDA) has granted EUAs to five anti-SARS-CoV-2 MAB medicines, including:

Due to the Omicron VOC’s significantly decreased in vitro sensitivity to Bamlanivimab and Etesevimab, these neutralising MABs bind to a variety of overlapping epitopes in the spike protein RBD of SARS-CoV-2. It is not anticipated that Bamlanivimab with Etesevimab would provide any therapeutic benefits for patients with Omicron infection as its distribution in the United States has been stopped.⁸⁷

This recombinant human protein neutralises MAB and binds to the advanced SARS-CoV-2 protein. There are no clinical efficacy data on the use of Bebtelovimab in patients at high risk for developing severe Omicron subvariants, despite the fact that it still has in vitro activity against all circulating subvariants of COVID-19.⁸⁸

These human MABs are recombinant, and they bind to nonoverlapping epitopes on the spike protein RBD of the SARS-CoV-2 virus. It is unlikely that Casirivimab and Imdevimab would provide any therapeutic benefit to patients with Omicron infection because the Omicron VOC’s in vitro susceptibility has been considerably reduced and its dissemination has been stopped.⁸⁹

This MAB contracted SARS-CoV in 2003. The Panel no longer recommends treating COVID-19, and Sotrovimab distribution has stopped.^90–92 Although it targets an epitope that both SARS-CoV and SARS-CoV-2 share in the RBD of the spike protein, the Omicron BA 2 subvariant is immune to it.⁹³

The non-overlapping epitopes on the spike protein RBD of SARS-CoV-2 are where these anti-SARS-CoV-2 recombinant human MABs bind. The FDA updated the EUA to authorise a dose of 300 mg each of the anti-cancer drugs ixagevimab and cilgavimab, which is expected to continue to work against all subvariants, including Omicron.^93–95

When critical SARS-CoV-2 patients experience a cytokine storm, which is an increase in pro-inflammatory cytokines, Tocilizumab, a monoclonal antibody made from recombinant anti-human interleukin (IL)-6 receptor, stops subsequent inflammatory cascades from occurring.⁹⁶ Therefore, it may be able to save individuals with severe COVID-19.⁹⁷

Another way of constricting COVID-19 is its prevention by vaccination. The approved vaccines listed under the Emergency Use Listing (EUL)⁹⁸ as of 2022 are shown in Table 2.

The BNT162b2 vaccine, developed by BioNTech, relies on the use of nucleoside-modified mRNA (modRNA), which encodes a mutated version of the full-length spike protein found on the surface of the SARS-CoV-2 virus.⁹⁹ This immune response is triggered in response to the virus protein, protecting the body from infection. It is encapsulated in lipid nanoparticles.¹⁰⁰ The Food and Drug Administration (FDA) in the United States approved the Pfizer-BioNTech vaccine as the first COVID-19 vaccination for individuals aged sixteen and older.^101–103

It is an adenovirus vector from a chimpanzee that is recombinant and replication-deficient and that encodes the spike(S) glycoprotein of the SARS-CoV-2 virus. After being administered, a portion of the corona virus’ genetic material is expressed and triggering an immunological reaction. Patients should not use covishield if they have low platelet counts in addition to venous and/or arterial thrombosis (thrombocytopenia). People with thrombocytopenia, anyone with a clotting condition, or those taking anticoagulant medication should use covishield with caution because, in these cases, intramuscular injections may result in bleeding or bruising.¹⁰⁴

The Jcovden brand of the COVID-19 vaccine, manufactured by Johnson and Johnson, it is a viral vector vaccine that is based on a human adenovirus modified to carry the gene that produces the spike protein of the SARS-CoV-2 virus that causes COVID-19.¹⁰⁵ The body’s immune system produces antibodies in response to this spike protein¹⁰⁶ with only one dose.

The Spikevax brand of the Moderna COVID 19 vaccine (INN: elasomeran). is a mRNA vaccine made of lipid nanoparticle-coated nucleoside-modified mRNA (modRNA) that encodes the SARS-CoV-2 spike protein.^107–108 Australia is authorised for the use of other brand of a bivalent vaccination called Spikevax Bivalent Zero/Omicron¹⁰⁹which contains elasomeran/elasomeran 0-omicron.¹⁰⁹

Sinopharm BIBP is one of two entire inactivated virus COVID-19 vaccines created by Sinopharm Beijing Institute of Biological Products is also known as BBIBP-CorV,¹¹⁰ the Sinopharm COVID-19 vaccine, or BIBP vaccine.^111–113 The inactivated viral vaccines for COVID-19 CoronaVac and Covaxin, as well as BBIBP-CorV, have comparable technology.¹¹⁴ The World Health Organization (WHO) suggested a gap of 3 to 4 weeks between dosages¹¹⁵ of this vaccine.

Sinovac Biotech, a Chinese Company created CoronaVac, also known as the Sinovac COVID-19 vaccine, which is a whole inactivated COVID-19 vaccine. Similar to Covaxin and the Sinopharm BIBP vaccine,¹¹⁶ is an inactivated-virus COVID-19 vaccine that uses conventional technologies. There are two dosages in the initial course. 4 weeks should elapse between dosages, according to the World Health Organization (WHO). Booster dose may be required after the initial course because preliminary data indicated that immunity dwindles quickly.¹¹⁷

The Indian Council of Medical Research (ICMR)-National Institute of Virology collaborated with Bharat Biotech to create Covaxin, an indigenous COVID-19 vaccine (NIV). SARS-CoV-2 particles that have been chemically deactivated are present in the inactivated whole virus vaccination known as Covaxin. That implies they are no longer able to infect cells but can still activate the immune system to defend itself. It is advised to space out the two doses of the vaccine by 28 days. Covaxin’s primary side effects were discomfort at the injection site, followed by headache, exhaustion and fever. There were no severe or fatal adverse effects reported with this vaccine.^117,118

The protein-based vaccination, Novavax has been given preliminary approval by the TGA for use in Australia. Part of the coronavirus spike protein is present in this kind of vaccine. Immunological system cells see the spike protein as a threat and start to mount an immune defence against it.¹¹⁸

Apart from treatment by different drugs and immune protection by vaccine, one can also get resistance power against viral attack by immune boosters in the form of nutrients as discussed below.

A fat-soluble steroid hormone, vitamin D, is converted into the circulating precursor cholecalciferol, which improves innate cellular immunity by inducing the synthesis of anti-microbial peptides including cathelicidin and defensins.¹¹⁹ Vitamin D insufficiency has been linked to both the likelihood and severity of COVID-19 infection. It has repeatedly been shown that COVID-19 patients have lower vitamin D levels than controls, with mean plasma concentrations that are only half as high.¹²⁰ Supplementing with vitamin D is suggested to improve immunity to COVID-19 and reduce death rates.¹²¹ Upper respiratory tract infections are negatively correlated with serum 25-hydroxyvitamin D levels. The incidence and severity of viral infection are therefore known to be reduced by vitamin D supplementation.^118–120 Its supplementation may reduce pro-inflammatory cytokines in people with COVID-19, hence reducing mortality from acute respiratory distress syndrome.¹²¹

To Neutralise Reactive Oxygen Species, Vitamin C works as an antioxidant (ROS), preventing oxidative damage and malfunction to biomolecules like proteins, lipids, and nucleotides.¹²² In addition to avoiding viral infections, Vitamin C is lowering their duration and intensity and supporting respiratory defence mechanisms with antihistamine characteristics that can lessen flu-like symptoms.¹²³ Vitamin C supplementation is beneficial for those who are lacking in micronutrients and at risk of contracting COVID-19 infection because it helps to prevent and strengthen immune responses.¹²⁴

Due to its dual immunomodulatory and antiviral properties, zinc is thought to be a crucial component during COVID-19 infection.^125,126 In patients with COVID-19, it is a viable supportive treatment. to lower respiratory tract infections, and other symptoms of COVID-19.¹²⁷

It is well known that the polyunsaturated fatty acids known as omega-3 fatty acids—which also include eicosapentaenoic and docosahexaenoic fatty acids—have advantageous effects on immunity and inflammation. Patients with COVID-19 may benefit from using omega-3 fatty acids to increase oxygenation.¹²⁸

The plant-based compounds can also be used to boost the immunity, as given below.

Curcumin exhibits a wide range of biological effects, such as antibacterial, antiviral, antifungal, antioxidant, and anti-inflammatory ones.¹²⁹ By preventing virus entry into cells, viral protease encapsulation, preventing virus reproduction and regulating a number of signaling pathways, it has an antiviral effect.¹³⁰ As a result, curcumin may be used as a supplement to fight against pathogenesis of COVID-19.

The essential oils of cinnamon contain large amounts of cinnamonaldehyde, a naturally occurring bioactive molecule^131–133 with possible anti-inflammatory properties, so may be helpful in reducing lung hyperinflammation brought on by SARS-CoV-2.

Allicin, the primary thiosulfate in fresh garlic extract, has demonstrated a range of health benefits as a result of its anti-inflammatory, antioxidant, and antiviral activities.¹³² In order to prevent COVID-19, fresh garlic extract may be helpful.

Black pepper’s primary alkaloid, Piperine, which is derived from its ethanolic extract belongs to the family of compounds known as cinnamides. Since Piperine has a potent anti-inflammatory effect, it can be used to control the hyperinflammation in COVID-19.¹³³ Piperine can therefore be utilised therapeutically or prophylactically to guard against the oxidative stress and hyperinflammation brought on by the COVID-19.

SARS-CoV-2 was effectively combatted by ginger and its bioactive components. Ginger’s bioactive components prevent SARS-CoV-2 entrance by blocking the spike (S) protein during infection.¹³⁴

They have insecticidal, antibacterial, antiviral, larvicidal, antimalarial and spermicidal properties.^135,136 Methyl eugenol, oleanolic acid and ursolic acid, are derived from tulsi and neem, respectively, are natural bioactive substances that inhibit SARS-CoV-2 by binding to the spike glycoprotein, RNA polymerase, and/or its protease and preventing both viral attachment and reproduction.¹³⁶

Selenium is widely distributed in everyday foods such as corn, garlic, onion, cabbage, and broccoli. It is a necessary micronutrient is crucial for several physiological functions as well as the immune system. Supplementing with selenium may be beneficial in the fighting against COVID-19 due to its significant impact in reducing inflammation, boosting antioxidant status and innate immunity.^137–140

Propolis, which is produced by honeybees, has a variety of biological properties, including anti-microbial, anti-inflammatory, dermatoprotective, laxative, anti-diabetic, anti-tumor, and immunomodulatory activity.^140,141 Propolis can be used in conjunction with antiviral and immunomodulatory effects to help for prevention of COVID-19.

Bifidobacterium and Lactobacillus species are the most widely utilised probiotics, followed by Streptococcus, Enterococcus, Bacillus, and Escherichia coli.¹⁴² The host’s innate immune response is improved by these probiotics, which also have anti-inflammatory properties, and the enterocytes and gut involvement¹⁴³ can act as reservoirs for SARS-CoV-2 infection. To combat the pathogenesis of COVID-19, probiotics can be utilised as adjuvants and preventatives.

The term “lactoferrin” refers to a safe and naturally occurring glycoprotein (Lf). It is necessary to prevent the virus from entering the body and proliferating.¹⁴⁴ By increasing T-cell activation, lowering interleukin levels like IL-6 and TNF-, and downregulating ferritin, it has immunomodulatory and antioxidant effects.¹⁴⁵ Additionally, it lessens the oxidative harm that H₂O₂ causes to the endothelial cells in the human umbilical vein.¹⁴⁶ As a result, it is used as a possible therapy and preventative approach for COVID-19.

Antiviral and anti-inflammatory effects can be found in the well-known antioxidant quercetin.¹⁴⁷ Synergistic antiviral and immunomodulatory effects are produced against COVID-19 when vitamin C is coupled with it.¹⁴⁸ Consequently, it can be considered as a possibility for COVID-19 therapy and prevention.

The predominant symptom of COVID-19 is ‘decreased lung capacity’. So, from our ancient practices, the yogosannas can also be practiced for improving lung power further to decrease complication in COVID-19.

Some yoga exercises practiced to improve lung capacity are:

Anulom Vilom Pranayama or Alternate Nostril Breathing Technique of Yoga: This breathing technique offers a multitude of advantages, including increasing memory, respiratory and cardiovascular health and blood pressure regulation.
Ustrasana (Camel pose): Numerous benefits of this breathing technique include improved blood pressure control, respiratory and cardiovascular health, and memory enhancement.
Hasta Uttanasana (Raised arms pose): Hasta Uttanasana is renowned for enhancing respiratory capacity and lowering exhaustion and fatigue. It reduces tension and enhances the body’s blood circulation.
Bhujangasana: This asana lessens lower back discomfort while also enhancing oxygenation of the body. In addition, it helps for blood circulation.
Paschimottanasana (Seated Forward Bend): It works wonders to reduce tension and calm the neurological system by calming the mind. It also lessens tiredness.

Though, the above preventive and treatment strategies used or can be used, the following Table 3 treatment packages are being prescribed during COVID-19 treatment.

Different demographics, genders, ABO blood types, HLA genotypes, groups of people of a certain ethnicity, and geographical origins have significantly different rates of COVID-19 incidence, severity and death. Because of this, finding a successful preventive approach has therefore been a primary focus, leading to the creation of large number of management strategies. So, still there is a need to propose different strategies based on advanced technology, knowledge or information gained about virus.

Gene therapy is one of the novel therapeutic approaches which employs genes or short oligonucleotide sequences as therapeutic molecules into cells to alter the phenotypes permanently. It is an approach to treat diseases either by modifying the expressions of specific genes or the rectification of abnormal genes. It can be accomplished by substituting the mutated gene with a new gene into the body. The major purpose of gene therapy is to introduce a functional gene into a person who has the deficiency of a specific gene and also to replace a missing enzyme to a patient who lacks a specific enzyme. Gene Therapy works by Gene Cloning, Carriers/ Vectors – like plasmids, Cosmides, phage virus, etc.

Airway cell gene expression could be altered by exposure to the SARS-CoV-2 spike protein.⁵⁹ The information about genetic expressions and the alleles that are involved for COVID-19’s susceptibility opens up new possibilities for designing a gene therapy for the disease. Genes that are heavily associated with cancer, viral infections, and autoimmune illnesses have been silenced via the RNA interference (RNAi) method.^149,150 When siRNAs targeted to the SARS-CoV-2 genes are characterised and analysed in vitro, a suitable in vivo transport approach must be chosen¹⁵¹ for the treatment of COVID-19. The created siRNA should be administered in this case via the pulmonary route, including inhalation, intranasal administration, and intratracheal aerosol delivery.¹⁵² When combined with anti-mucosal medications, aerosol administration of lipidic, polymeric peptide, or inorganic siRNA derived nanocarrier systems may be able to overcome limitations such neutrophil and macrophage degradation.¹⁵³ Some of the molecular biology methods that can be used to manage illnesses like COVID-19 or pandemics include gene editing techniques like CRISPR-Cas12/13-based SHERLOCK, DETECTR, CARVER and PAC-MAN, ASO, antisense peptide nucleic acids, ribozymes, aptamers, and RNAi silencing treatments.¹⁵⁴ These techniques were developed with cutting-edge scientific developments.

COVID-19 has already professed as a global pandemic and health emergency by the WHO, this enduring crisis has driven the progress of effective therapeutic agents thus resulted in testing of repurposed drugs. Currently, the speed of infection spread has partially halted through vaccination but, some of the breakthrough infections are reported even in fully vaccinated individuals. To deliver an optimized treatment, different biomarkers have been studied¹⁵⁴ and critical biomarkers can predict the severity of COVID-19.¹⁵⁵ The medications currently used to treat COVID-19 can cause more side effects. One treatment may not be appropriate for everyone due to these adverse effects being genetically unpredictable amongst different people. These considerations allow the personalised therapy to more potently lessen the existing epidemic.¹⁵⁵ The use of personalized medicine is also suggested for COVID-19 treatment.¹⁵⁶ Due to the heterogenicity in the host responses to the COVID-19 condensed and personalized treatment is essential to gain promising consequences. Through an extensive array of genomic and proteomic investigation, the identification of specific immune responses can be accomplished in segregating the population. This leads to more specific treatment and an improved response to the therapy. Clinical and paraclinical variables can be used to evaluate the dynamics of the illness and the likelihood that it will advance to more severe manifestations. Depending on when the condition first appeared, the goal would be to start the best possible treatment regimens. In this sense, managing COVID-19 patients ideally moves beyond the simplistic notion of “one disease, one treatment” and instead emphasises “a disease with a clinic-biological form, a particular kinetics, and therefore a particular treatment”.¹⁵⁶

Patients with severe forms may be admitted to the hospital at the beginning of the illness, when the viral phase is crucial, or, more usually, during the inflammatory phase, a week after the illness begins.¹⁵⁷ Some of these people will have biological inflammatory signs that are more noticeable than others. Thus, in the management of the disease can be possible by some targeted Novel drug delivery systems to decrease side effects and future complications with the existing treatment strategies. The development of pulmonary targeted drug delivery systems using nanotechnology also emphasises the effective management of lung capacity.¹⁵⁸

The COVID-19 pandemic is still having an adverse effect on the world, and its long-term effects are still not known. In this day and age, it is sad that there are still so many communicable diseases, but fortunately, they may be overcome. With the aforementioned sudden unfortunate situations in mind, people must strengthen their innate immunity to fight or resist against such diseases. To do this, people have been taking immune boosters and vaccines since birth and avoiding junk food, processed foods, and other things that affect or weaken human immunity. Identifying high-risk biomarkers, which may potentially offer possible targets for treatment, requires taking into account the link between the host genetic base and COVID-19. New therapeutic technologies that are rapid, accurate, stable, easy to manufacture, and target specific for surveillance and therapy are urgently needed, as shown by the emergence of the novel coronavirus.