1. SARS-CoV-2
Coronaviruses under the realm of Riboviria belongs to the order Nidovirales, suborder cornidovirinea, family Coronoviridae [
1]. Orthocoronavirinae the subfamily of coronoviridae is further divided into four genera alpha (a), beta (b), gamma (c), and delta (d) coronavirus. Further, SARS-CoV belongs to Beta coronavirus and sarbecovirus is the subgenus of SARS-CoV-2 [
2]. It shares similar homology with bat coronavirus and it has been estimated that both have 96.2% sequence homology [
3].
The two epidemics due to coronavirus have already occurred that were due to SARS-CoV and the Middle East respiratory syndrome (MERS) and both have been the major cause of pneumonia in humans [
4]. SARS-CoV emerged in 2002 and remained till 2003 during the period it caused 774 death and more than 800 people were infected. MERS-CoV emerged in Saudi Arabia in 2012, which caused more than 800 deaths, and 2500 people became infected [
5].
Coronaviruses have single-stranded RNA as genetic material that can range from 26 kbs to 32 kbs in length. Coronaviruses possess specific genes in Open Reading Frame ORF1 downstream region that are responsible for encoding the proteins responsible for viral replication, nucleocapsid, and spike formation [
6]. The structure of SARS-CoV shows the spikes on the outer surface. Furthermore, studies have shown that structural proteins are encoded by the four structural genes, which include spike (S), envelope (E), membrane (M), and nucleocapsid (N) gene. These genes are responsible for viral functionality and structure [
7].
SARS-CoV-2 genome is 80% similar to the previous human coronavirus SARS-CoV [
8]. For some of the encoded proteins such as coronavirus main proteinase (3CLpro), papain-like protease (PLpro), and RNA-dependent RNA polymerase (RdRp) the sequence similarity is very high (96%) between SARS-CoV, and SARS-CoV-2 [
9].
SARS-CoV-2 and SARS-CoV spike protein have 76.5% identical amino acid sequences [
10]. The 3D structures of spike proteins of SARS-CoV-2 and SARS-CoV as analyzed by computer imaging revealed that both have identical structures in the receptor-binding domain and maintains the Vander Waals force [
10]. The major amino acid residue of SARS-CoV-2 in the receptor-binding domain is Gln-493, which favors the attachment of spike protein S with human cells more specifically with the lungs therefore the attachment results in respiratory infections in humans [
11,
12]. Zhao et al. [
11] have suggested that 83% of the angiotensin-converting enzyme (ACE-2) expressing cells are alveolar epithelial type II, therefore, these cells can be the reservoir for the viral invasion. Some analysts have suggested that SARS-CoV-2 binds to ACE-2 more efficiently as compared with SARS-CoV, therefore, it has a greater ability to transmit from person to person [
13].
Initially, for the attachment to the host cells, virus use the spike (S) glycoprotein, which also mediates the host and viral cell membrane fusion during infection [
14]. The spike (S) glycoprotein has two regions namely S1 and S2. S1 helps in the binding of host cell receptors, and S2 helps in the fusion with the membrane. The receptor-binding domain (RBD) is located in the S1 region of SARS-CoV and the attachment of the human host cell with the virus is mediated by the RBD protein of the RBD domain with the angiotensin-converting enzyme (ACE-2) as a receptor similar to the one required by SARS-CoV [
15,
16]. Since SARS-CoV and SARS-CoV-2 are much similar, it is believed that SARS-CoV-2 uses a similar receptor (ACE-2) for entering into human host cells [
10,
13].
The initial clinical symptoms that appear after SARS-CoV-2 infection are pneumonia, fever, dry cough, headache dyspnea, and in acute cases leads to respiratory failure and eventually, death occurs [
17,
18,
19]. Although the healing depends upon immunity, pre-existing conditions such as hypertension, diabetes, cardiovascular diseases, or kidney diseases further enhances the severity of the pathogenesis of SARS-CoV-2 [
17,
19]. Different drugs are available in the market against SARS-CoV-2 but none has shown accurate results. None of the drugs has been approved by FDA against SARS-CoV-2.
Plants have been used as a medicine in the traditional Chinese and Ayurvedic systems [
20]. Some of the herbal medicines have safety margins above those of reference drugs, which shows that they can be used against mild SARS-CoV-2 infection [
21]. Plants in the form of herbal medicine or dietary components act as immunomodulators and can be a potent antiviral against SARS-CoV-2 infection [
22].
Medicinal plants contain diverse secondary metabolites, therefore, they have been the source of drugs against viral, bacterial, and protozoal infection, including cancer [
23,
24]. The secondary metabolites present in the medicinal plants can interrupt viral proteins and enzymes by binding with them and preventing viral penetration and replication [
25,
26,
27,
28]. When consumed without knowing the appropriate dosage, herbal medicines may be toxic [
29]. The genetically modified (GM) plants also pose serious health issues because the unnatural change in naturally occurring protein or the metabolic pathways results in toxins or allergens [
30]. Therefore, the selection of medicinal plants is also an important aspect.