Table 1.

Probable strategies against COVID-19

No.	Probable strategy against COVID-19	Mechanism of action of potential strategy	References
1	DNA vaccine (INO-4800)	Stimulates T cell activation by introducing plasmid DNA which displays the spike of SARS-CoV-2	[2]
2	Hyleukin-7 Technology-based COVID-19	Immune reactions are improved by combining interleukin-7 (IL-7) to hy-Fc, hybridizing IgG4 and IgD where unexposed junction area of IgG4 helps reduce detrimental immunogenicity	[2]
3	Recombinant subunit vaccine	An indigenous trimeric viral spike to which the presence of antigen-specific neutralizing antibodies was validated	[2]
4	Protein subunit vaccine	A molecular clamp secures a surface protein, enhancing the identification of an appropriate antigen which results in better immune responses	[2]
5	Inactivated SARS-CoV-2 vaccine	Containing an entire particle of virus that is inactivated chemically with the addition of immune system booster termed as alum into this vaccine	[8]
6	Viral vector-based vaccine -Adenovirus type 5 vector vaccine (Ad5- nCoV)	Contained in this vaccine is an adenovirus 5 present in non-replicating form which plays the role of a vector in order to transfer the SARS-CoV-2 spike protein’s gene	[8, 9]
7	ACE-2 inhibitor	Enalapril and captopril may inhibit SARS-CoV-2 entry in patients suffering from SARS-CoV-2-induced-pnemunia	[11]
8	Protein S-centered vaccines	Protein S-centered vaccines based on S1-RBD or complete-length protein S would produce antibodies that inhibit viral receptor’s attachment and its genome’s uncoating event	[12–14]
9	Epitope-based vaccine	Epitopes of CTL (cytotoxic T lymphocytes) can attach to peptide-binding grooves of MHC class I, implying their ability to generate immune responses	[13]
10	Humanized nano-bodies and human antibodies	Attach to or intervene with the biological activity of viral proteins e.g. 3CLpro (cysteine-like protease), PLpro (papain-like protease) and Nsps (non-structural proteins) that are being replicated, hence impeding viral replication and transcription	[13, 35]
11	Epitope-based vaccine	E protein’s possible B cell epitopes and Nucleocapsid (N) protein of MERS-CoV can elicit neutralizing antibody reactions and responses of T-cell	[17, 18]
12	Live-attenuated vaccine	Deploying reverse genetic techniques to disable the non-structural protein 14 exonuclease consequences or remove the SARS envelope protein	[19]
13	Antigen-based vaccine	RBD-FP fusion protein has been developed that has shown to produce a large titer of antibodies in mice	[20]
14	Live-attenuated vaccine	Codon deoptimization process on virus is carried out or employed to produce a live-attenuated SARS-CoV-2 vaccine	[20, 21]
15	mRNA vaccine (mRNA-1273)	LNP-enclosed protein S mRNA gets delivered into cytoplasm where protein S translation occurs, thus triggering cellular and humoral immune reactions	[20, 24]
16	Plant-based chimeric protein and subunit vaccines	Using plants to generate complete-length viral surface proteins found in the envelope area, chimeric proteins or subunit vaccines and monoclonal antibodies against ACE2 at a faster pace	[22]
17	Antigen-based vaccine	M-protein transmembrane domain comprises a T-cell epitope cluster capable of inducing a potent cellular immune response	[28]
18	Intravenous immunoglobulin (IVIG) infusion therapy	From sera of convalescent individuals with the viral infection, IVIG could be derived from which IgG could be obtained, transmitting normal innate immune system to compromised individuals	[29]
19	Vitamin D	Vitamin D might restrict the CoV spread by inhibiting the receptor ACE-2 through regulation of angiotensin-renin mechanism which might alleviate lipopolysaccharide-provoked severe lung injury	[30, 31]
20	Angiotensin 1 receptor (AT1R) inhibitor	Using antagonists of AT1R like telmisartan and losartan to disable immoderate angiotensin-conciliated AT1R activity that has been fueled via virus infection	[32]
21	Complement system inhibitors	For repulsing complement activation, inhibitors of C3 can be deployed which can concomitantly impede C5a and C3a synthesis, thus improving injury in lungs	[33]
22	Carmofur Antiviral drug	SARS-CoV-2 main protease when bound with carmofur has the ability to directly alter catalytic Cys145 of main protease of SARS-CoV-2, thus inhibiting its main protease and hindering its replication	[41]
23	Endovenous mesenchymal stem cell (MSC) infusion	MSC infusion can minimize excessive immune system activation and promote recovery by regulating the lungs microenvironment	[42, 43]
24	Shield immunity	Through interaction substitution, the recuperated subjects who possess antibodies should interact with infected and vulnerable subjects, aiding to introduce ‘shield immunity’ at the level of community	[50]
25	hACE2-SARS-CoV-2-RBD interaction blocking monoclonal antibody	Two blocking, human mAbs have been cloned which could attach to RBD of SARS-CoV-2, hence obstructing the contact between receptor hACE2 and RBD of SARS-CoV-2	[51]
26	IL-6R blocking monoclonal antibody	Tocilizumab, antagonist of IL-6R, can attach to transmembrane and soluble forms of IL-6R, inhibiting the intracellular signaling pathway that leads to CRS (Cytokine Release Syndrome) which is caused by SARS-CoV-2 in severely affected patients	[52]
27	CD94/NK group 2 member A (NKG2A) blocking monoclonal antibody	To counter inhibitory activity of NKG2A which quells the immune cell’s cytotoxic functionality, monoclonal antibody against NKG2A namely monalizumab is being experimented	[55]