Traditional Ayurvedic 

Formulation In The Management of COVID-19.

Abstract:

Coronavirus disease 2019 (COVID-19) is a new infectious disease caused by severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2) that belongs to the coronavirus family.
The first case was reported in December 2019, and the disease has become a pandemic.
Impaired immune regulation is one of the factors that play a role in its pathogenesis and
results in poor outcomes of COVID-19 patients. There have been many studies with drug
candidates used as antivirals or immunomodulators. However, the results of these
investigations showed that the drug candidates were not significantly effective against the
disease. Meanwhile, people believe that consuming herbal immunomodulators can prevent or
even cure COVID-19. Unfortunately, specific preclinical and clinical trials to evaluate the
effects of herbal immunoregulators have not been conducted. Certain natural compounds
might be effective for the treatment of COVID-19 based on general concepts from previous
experiments. This review discusses some herbal agents extracted from various plants,
including Echinacea, Cinchona, Curcuma longa, and Curcuma xanthorrhiza, which are
considered for the treatment of COVID-19. In addition, we discuss the pros and cons of
utilising herbal medicine during the COVID-19 pandemic, draw some conclusions, and make
recommendations at the end of the session.
Introduction:

COVID-19 was announced as a pandemic on 11 March 2020 by WHO[1], leading to the

rapid spread of novel coronavirus (COVID-19) into a pandemic responsible for the current
global health crisis[2]. The actual number of infected cases is probably much higher due to
asymptomatic cases that may be responsible for the development of the pandemic. In
February 2021, there have been more than 117 million confirmed cases of COVID-19 and
more than 2.6 million deaths worldwide, as reported by the WHO3. The coronavirus outbreak
was caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). SARS-CoV-
2 is an RNA virus with a similar genetic structure to that of SARS-CoV or MERS-CoV.
Protease which is encoded by the viral genome, plays a crucial role in the production of viral
proteins, and Controlling the function of the replicase complex, which is required for virus
replication and infection, makes it the perfect target for designing antiviral therapies. Acute
respiratory syndrome (SARS-CoV) coronavirus enzymes are one of the most promising
targets for the discovery of anti-SARS drugs because of their key role in the life cycle of the
virus[4].

This analysis aims to present historical data on the antiviral activity of a specific herbal
medicine against SARS-CoV-2. This will promote the use of herbal medicine as
complementary COVID-19 prevention therapies, given the current absence of an effective
drug or vaccine against SARS-COV-2. Many other doctors and researchers have already tried
clinical trials with herbal medicines to suppress SARS-CoV-2[5].

Structure of SARS-CoV-2:

As a novel betacoronavirus, SARS-CoV-2 is one of the viruses that belong to coronaviruses.

It is a positive single-strand RNA virus (+ssRNA) belonging to the order Nidovirales, family
Coronaviridae, and subfamily Orthocoronavirinae[6]. This specific coronavirus is categorized
into four genera: α, β, γ, and δ. Each genus is further subdivided based on subtype, genome,
and phylogenic clustering characteristics. Humans are actually infected with six distinct
forms of coronavirus. As a result, SARS-CoV-2 is now the seventh coronavirus capable of
infecting humans. SARS-CoV and MERS-CoV (Middle East respiratory syndrome
coronavirus) that infect humans belong to the β genus that is a predecessor for the SARS-
CoV-2. The other forms of human coronaviruses are 229E and NL63 that belong to the α
genus and also OC43 and HKU1 that belong to the β genus[7,8].
The RNA of this novel SARS-CoV-2 is ∼30 kb long, the same length as that of the SARS-
CoV and MERS-CoV viruses that caused problems several years ago. SARS- CoV-2 shares
79% genome sequence identity with SARS- CoV and 50% with MERS- CoV[9]. Its genome
structure is similar to that of other betacoronaviruses. Replicase (ORF1a/ORF1b), spike (S),
envelope (E), membrane (M), and nucleocapsid (N) are the six functional open reading
frames (ORFs) organized in order from 5′ to 3′[10].SARS- CoV-2 shares more than 90%
amino acid identity with SARS- CoV except for the S gene, which diverges[9,11]. Most of
these SARS- CoV-2 non-structural proteins have greater than 85% amino acid sequence
identity with SARS- CoV[10].

Coronaviruses have a pleomorphic, circular, or oval envelope. This virus measures 50–200
nanometers in diameter[6,8]. SARS-CoV-2 has a peculiar spike projection on its surface that
resembles a solar corona[6,8]. This newly discovered coronavirus encodes four large
structural proteins that are spike (S), membrane (M), envelope (E), and nucleocapsid (N). The
most important structure capable of binding to the receptor is the S protein. This
glycoprotein, which is found on the virus's surface, is responsible for the virus's attachment to
the receptor on the host cell[8,12]. In this virus, this protein also serves as the virus's primary
antigenic structure[7]. This virus's S protein is a trimeric S glycoprotein, a class I fusion
protein that mediates binding to the receptor of the host cell.

The S protein of SARS-CoV-2 can interact strongly with the host cell via the ACE2 receptor
as same as SARS- CoV, angiotensin-converting enzyme 2 (ACE2). This interaction poses a
risk of human transmission to public health[6,7]. After the binding of s protein of the virus
with ACE2, the envelope of virus fuse with the host cell membrane and enter the host cell
[6,12].

Heading:

 A recent travel to or residence in epidemic regions

Epidemiology: within 14 days.
 Contact with cases from other epidemicregions or
symptomatic cases.
 Clustered cases or having contact with confirmed
cases.
 Fever, Loss of taste and smell, difficulty in
Clinical sign: breathing.
  Dry cough,sore throat.
 Radiologic characteristics consistent with
pneumonia.
 Normal or decreased leukocyte count at early stages,
or lymphopenia.
 Detection of SARS-COV-2 or homology of SARS-
COV-2 in the respiratory tract or blood specimens.
Pathogen and  Detection of the virus nucleic acid by real-time
Diagnosis: reverse transcription polymerase chain reaction
(rRT-PCR), transcription-mediated amplification
(TMA), or by reverse transcription loop-mediated
isothermal amplification (RT-LAMP) from a
nasopharyngeal swab.

Pathophysiology:

The spike glycoprotein-S bind to angiotensin converting enzyme -2 (ACE-2) receptors cells
which help SSRNA to enter the host cell [13]. where translation occurs and formation of
polyproteins whichwill cleave by using TMPRSS2 (transmembrane protease serine 2) to
make viral components along with SSRNA has potential to use another enzyme which is
RNA dependent RNA polymerase to replicate the SSRNA [14]. So, both replicated SSRNA
and viral components joined to form virus (COVID- 19) which signals to release the
macrophage upon tissue damage than the other inflammatory mediators(IL-6, IL-10, Tumour
necrosis factors, granulocyte colony-stimulating factor, monocyte chemoattractant protein 1,
macrophage inflammatory protein 1, are released from endothelium layer [15].which will
cause the dilation of blood vessels by contraction of endothelium layer to increase the
capillary permeability that causes alveolar edema leads to drowning out surfactant that
responses to increases the surface tension the alveoli will collapse that tend to decrease the
gaseous exchange that leads to hypoxemia and increase the work of breathing that causes
dyspneai.e shortness of breath.

All inflammatory mediators bring neutrophils from blood to alveoli to destroy the virus by
releasing reactive oxygen species (ROS)and protease which damages all cells including
(ACE- 1 and 2) and the results sloughing off. Damage cells along with the consolidation of
fluid accumulation, protein deposition, and cellular debris alter the gaseous exchange to
promote hypoxemia. This causes septic shock the patient becomes hypotensive, decreased
total peripheral resistance, blood pressure, and decreased perfusion of their organs. it will also
affect the liver to raise levels of AST, ALT, bilirubin, their response on the kidney is to
increase the creatinine levels. SARS CoV-2 binds to host cells through the ACE2 receptor,
which is expressed by epithelial cells of the lungs, intestine, kidneys, brain, and blood vessels
[16] which consequently promotes SARS-CoV-2 infection severity.

Ayurveda, being the science of life, propagates the gifts of nature in maintaining healthy and
happy living. Ayurveda’s extensive knowledge base on preventive care, derives from the
concepts of “Dinacharya” - daily regimes and “Ritucharya” - seasonal regimes to maintain
healthy life. It is a plant-based science. The simplicity of awareness about oneself and the
harmony each individual can achieve by uplifting and maintaining his or her immunity is
emphasized across Ayurveda’s classical scriptures. One of best ayurvedic preparation is
Kadha ( decoction )

Herbal drugs used in COVID-19:

Phytochemicals commonly used herbs in making Kadha Some of the commonly used herbs
in the preparations of Kadha includes Tulsi (Ocimum sanctum), Haldi (Curcuma longa),
Giloy (Tinospora cordiofolia), Black pepper (Piper nigrum), Ginger (Zingiber officinale),
Clove (Syzygium aromaticum), Cardamom (Elettaria cardamomum), lemon (Citrus limon)
and Ashwagandha (Withania somnifera). A list of 108 phytochemicals present in herbs that
are used in the preparation of Kadha or similar drinks were collected from the literature.
Phytochemicals found in Ocimum sanctum (Oleanolic acid, Ursolic acid, Rosmarinic acid,
Eugenol, Carvacrol, Linalool, Beta-caryophyllene, Estragole, Eugenic acid, Apigenin,
Cirsimaritin, Isothymusin, Isothymonin, Vicenin, Orientin and Cirsilineol) (Pattanayak et al.,
2010), Curcuma longa (Curcumin, Demethoxycurcumin, Bisdemethoxycurcumin, Ar-
turmerone, Alpha-turmerone, Beta-turmerone, Atlantone, Cyclocurcumin, Calebin A, Trans-
Ferulic acid, Vanillin and Vanillic acid) (Li et al., 2011), Tinospora cordiofolia
(Magnoflorine, Berberine, Choline, Jatrorrhizine, Beta-Sitosterol, Tinosporide,
Tinosporaside, Cordifolioside A, Tinocordioside, Cordioside, Tinocordifolioside and
Tinocordifolin) (Sharma et al., 2019), Piper nigrum (Piperine, Piperamide, Piperamine,
Pipericide, Sarmentosine, Sarmentine, Brachyamide B, Dihydropipericide,
NFormylpiperidine, Guineensine, Pentadienoylpiperidine, Tricholein, Trichostachine,
Piperettine, Piperolein B, Retrofractamide A, Chavicine, Isochavicine, Isopiperine, Nerolidol,
b-caryophyllene and Piperic acid) (Damanhouri & Ahmad, 2014), Zingiber officinale (6-
gingerol, 6-shogaol, 6-paradol, Zingiberene, Bisabolene, 1-dehydrogingerdione, 6-
gingerdione, 10-gingerdione, 4-gingerdiol, 6-gingerdiol, 10- gingerdiol, Citral and
Eucalyptol) (Bhattarai et al., 2018; Prasad & Tyagi, 2015), Syzygium aromaticum (beta-
caryophyllene, Vanillin, Eugenol, Acetyl eugenol, Crategolic acid, Eugenin, Methyl
salicylate, Kaempferol, Rhamnetin, Eugenitin, Oleanolic acid, Stigmasterol, Campesterol,
Gallic acid and Flavonol glucosides) (Cortes-Rojas et al., 2014), Elettaria cardamomum
(Protocatechualdehyde, Protocatechuic acid, Alpha-terpinyl acetate, 1,8-cineole, Linalool,
Linalyl acetate, Limonene, 4-terpineol and Geraniol) (Noumi et al., 2018), Citrus limon
(Eriodictyol, Quercetin, Hesperetin, Phloroglucinol, Umbelliferone, vitamin C (Vandercook
& Stephenson, 1966; Rangel et al., 2011) and Withania somnifera (Withaferin A,
Somniferine, Choline, Anaferine, Withanolide A, Withanolide B, Withanone and
Withanolide) (Sangwan et al., 2004). 3D structures of these different phytochemicals were
downloaded from PubChem (https://pubchem.ncbi.nlm.nih.gov) in structure-data file (SDF).
Preparation of Ayurvedic Kadha. There are specific Ayurvedic methods to prepare the
Kadha. In India, variants of standard Kadha are also prepared using different combinations of
herbs depending on the severity of disease/ailment and the availability of ingredients. The
most common ingredients are Tulsi leaves (10–15 leaves or 1=4 teaspoon powder), Ginger
(2–5 g rhizome or 1=4 teaspoon powder), Clove (4–5 pieces), Black pepper (4–5 pieces),
Cardamom (4–5 pieces), Ashwagandha (2–5 g raw or 1=4 teaspoon powder) and Giloy (2–5
g raw or 1=4 teaspoon powder). To make the Kadha, these herbs are boiled in 200 ml water
for 5–10 min, and jaggery or honey is added to make it sweet. The preparation is filtered and
mixed with 1=4 teaspoon of lemon juice. In case, if all ingredients are not available, it can be
prepared using locally available ingredients.

HERBS ACTIVE MECHANISM OF REFERENCE

COMPOUNDS ACTION
It acts as a possible
Curcumine, inhibitory agent blocking
Curcumin Demethoxycurcumine the host viral interaction Yamuna et al.
. (viral spike protein- ACE 2 (2020)
receptor) at a human entry
 site.

Quinine, Inhibiting NF-kB by

Cinchona Cinchonine, blocking the gene's Rhea et al.
Qunidine. expression, inhibit the (2020)
synthesis of the protein,
block microorganism
replication

Withaferin A,
Ashwagandha Withanolide (B,D), Inhibit SARS-Cov 2's main Priya et al.
Somniferine A, protease (Mpro or 3Clpro). (2020)
Withanosides (I–VII).

Forsythia suspensa,
Ephedra sinica  Stapf, Inactivate SARS-CoV-2
Lianhuaqingwe Lonicera japonica, replication, reduce pro- Li et al. (2020)
n Isatisindigotica, inflammatory cytokines
Mentha haplocalyx. production.

Turmeric:

Turmeric is a herbal plant also known as Curcuma longa (C. longa) belonging to the family
Zingiberaceae and the Curcuma genus. It is widely known as a medicinal plant to treat
various diseases and conditions. It contains carbohydrate (96.4%), protein (6.3%), fat (5.1%),
mineral (3.5%) and moisture (13.1%). Its extract contains curcuminoids, which are curcumin
(77.7%), demethoxycurcumin (DMC 17%) and bisdemethoxycurcumin (3%). The most
common curcuminoid that is used as a medication is curcumin [1]. It is the yellow pigment of
turmeric is widely used in our Indian Traditional herbal medicine to cure diseases associated
with inflammation and infections for many decades. It is also reported that curcumin exerts
antiviral activities.

According to recent research, the SARS-COV2 virus, like the original SARS-CoV, infects
human host cells by attacking the Angiotensin Converting Enzyme 2(ACE2) membrane
receptor, which is a coronavirus entry site. The viral S protein binds to the ACE2 receptor on
the mucus membrane, allowing for viral and membrane fusion and subsequent viral
replication in the host. ACE2 expression was found in nasal epithelial cells, pulmonary
alveolar epithelial type II cells (AECII), and the luminal surface of intestinal epithelial cells,
according to a recent report. Angiotensin-converting enzyme 2 (ACE2), a homologue of ACE
with 61 percent sequence similarity to the ACE catalytic domain, hydrolyses Angiotensin II
to Angiotensin (1–7) and attenuates Angiotensin II-ATIR axis mediated vasoconstriction
effects, lowering blood pressure via vasodilation.

In light of the growing evidence of curcumin's therapeutic properties, they propose a

hypothetical treatment strategy in which curcumin is used as:
1) A possible inhibitory agent blocking the host viral interaction (viral spike protein—ACE2
receptor) at a human entry site.
2)As a COVID19 attenuator, it reduces respiratory discomfort by modulating the
proinflammatory effects of Angiotensin II-AT1 receptor-signalling pathways.

Curcumin's function in the control of RAAS (renin-angiotensin-aldosterone system)

components, through which it is known to exert antioxidant, anti-inflammatory, and
antihypertensive effects, has also been extensively researched. Curcumin has been linked to a
reduction in the expression of ACE and AT1R receptors in brain tissue and vascular smooth
muscle cells in animal studies.

Inhibition of the symptoms of hypertension and oxidative stress induced by Angiotensin II-
AT1R in animals. Previous research has found high levels of AT2R and ACE2 expression in
myocardial cells treated with curcumin, indicating that curcumin can protect the heart by
modulating the effects of the Angiotensin II receptors AT1R and AT2R. Upregulation of
AT2R causes AT1R expression to be suppressed, resulting in anti-inflammatory effects
mediated by Angiotensin II-AT2R, including inhibition of NF-B activity and oxidative stress.
As a result, curcumin therapy reduced the proinflammatory effects of the Angiotensin II-
AT1R axis, resulting in substantial reductions in proinflammatory cytokines TNF-, IL-6 and
reactive oxygen species.

Cinchona:

Cinchona officinalis (Cinchona, Quinine), a member of the Rubiaceae family and the Genus
Cinchona, has been prized for its antimalarial properties for decades. [medicinal and aromatic
plt] Jesuit's bark, Peruvian bark, Cinchona bark are all synonyms for the cinchona. [IJCRT
journal] Cinchona bark contains approximately 30 different forms of quinoline alkaloids.
Quinidine, quinine, cinchonine, and cinchonidine are the most common alkaloids found in
cinchona bark. Quinine alkaloids make up 30-60% of the cinchona's composition. [IJCRT
journal] Cinchona trees (Cinchona L., Raiatea) from the Andean mountain forests have
several advantages, as a basic component of the trees contains bioactive compounds that can
help to cure fever. Jesuit missionaries were the first to notice this beneficial influence, which
spread across the world over time [51].

To treat COVID-19, quinine sulphate has been one of the most sought-after drugs in society.
State officials and physicians made insensitive remarks, causing widespread panic. As a
result, people searched out competitively quinine-containing drugs. Because of the high
incidence and mortality rate of COVID-19 globally, the people's behaviour was caused by a
spontaneous reaction. This section will go into how quinine can be used as an antiviral and
immunomodulator in a virus-related disease. Also, the potentially adverse effects of quinine
in people with or without COVID-19 will be discussed. Quinine gained popularity as a
substitute for the antimalarial medication chloroquine. Malaria medications were gradually
repurposed as potent inhibitors of viral infection, rather than as antimalarial drugs.
According to a large amount of evidence, many antimalarial drugs had been studied and
found to have some benefits against viral infection. [53].

Chloroquine, for example, had antiviral activity against the SARS-CoV infection.[54]
Seeleretal was the first to study the quinine effect as an anti-influenza virus infection
treatment.[55] Furthermore, Baronietal identified quinine's antiviral activity.Quinine sulfate
suppresses viral infection in indirect ways, for example, by inducing a heat shock protein
response, disrupting multiple pathways during virus replication, and inhibiting NF-kB by
blocking gene expression, according to a study that evaluated quinine sulphate on infected
HSV-1 HaCat cells.[56] Viruses infecting host cells cause viral RNA to be released,
disrupting normal protein synthesis. However, associate degree expression of an infective
agent recognition receptor (PRR) called RIG-I within the infected host cell will increase
minimally to promote the IFN-I signaling pathway instead of elevating organic phenomenon
of IFN-stimulated genes (RNase L, PKR) that inhibit the synthesis of the protein, thereby
block microorganism replication[58] In virus-infected cells, the RNase L pathway can
remove ssRNA, while PKR inhibits translation and interferes with signaling.[59] Infected
host cells' genome replication and translation are inhibited, and RIG-I and IFN are increased.
IFN is the cytokine secreted by host cells to combat viruses, according to research.[57]
Quinine sulphate works as an antiviral agent by boosting RIG-I and IFN-alpha production.
Both will then activate PKR to prevent viral mRNA translation and RNAse to degrade viral
poly mRNA (L) As a result, there is no viral protein produced. Since available data show that
quinine prevents the release of TNF- α, the most important cytokine in determining the
severity of COVID-19 symptoms, CSS does not appear in COVID-19 after quinine
administration. [60,61] Since quinine inhibits TNF- α expression at the mRNA transcription
level, as measured by northern blot, it will reduce rather than promote inflammation in
microbe-infected people.[60] While the cinchona tree extract does not cause CSS directly,
Lilesetal found that quinine can cause immune-mediated and toxic reactions.

In 2009, a Belgian research group reported the efficacy of chloroquine in eradicating lethal
viral infections caused by the human coronavirus OC43, which is closely linked to the human
coronavirus. Through injecting the drug into the mother's milk, SARS was able to spread
around the world. [medicinal and aromatic plt[36] In terms of the efficacy of chloroquine
against SARS-CoV-2, a recent study involving hundreds of COVID-19 patients found that
the chloroquine-treated group was superior in terms of reducing the duration of the disease
progression of the condition, strengthening lung imaging results, and pneumonia a
deterioration and an increase in virus-negative seroconversion Compared to the placebo
group, there were no side effects. .[medicinal and aromatic plt[37] The drug was given in a
500 mg dose twice daily in this first clinical trial against COVID-19. A multicenter
collaboration committee of the Department of Science and Technology and the Health
Commission of the United States released an expert consensus on February 20, 2020.
Chloroquine phosphate tablets are produced in the province of Guangdong.500 mg twice a
day for ten days is prescribed as a starting dose. mild, moderate, and serious cases of SARS-
CoV-2 pneumonia. .[medicinal and aromatic plt[38] Treatment victimization chloroquine
might enhance the treatment success rate, shorten the hospital keep, and lowers the mortality
related to COVID-19.

Ashwagandha:

Withania somnifera (Ashwagandha) is known to inhibit SARS-Cov 2's main protease (Mpro
or 3Clpro). Somniferine and Withanoside V were found to inhibit SARS-CoV-2 activity. The
main proteases of SARS-CoV-2 were studied as a potential macromolecular target for
COVID-19 management using active phytoconstituents from Ayurvedic scriptures.
Ayurveda, also known as "The Science of Life," is an ancient Indian philosophy of medicine
based on the holistic concept of life, wellness, and healing. The ayurvedic text describes a
group of rejuvenation methods that provide biological nourishment to body tissues (Singh et
al., 2008). It describes several medicinal plants with a wide range of therapeutic potential in
treating respiratory illnesses, one of which is Withaniasomnifera (Ashwagandha). Which acts
as an immunomodulator and helps the body fight infections.

W. somnifera (WS), also known as Ashwagandha, is a Rasayana (rejuvenator) that has been
shown to improve physical and mental well-being, rejuvenate the body in weakened
conditions, and increase longevity (Williamson, 2002). Anti-inflammatory, anti-diabetic,
antimicrobial, analgesic, anti-tumor, anti-stress, neuroprotective, cardioprotective,
rejuvenating, and immunomodulatory properties have been identified (Kapoor, 1990; Ven
Murthy et al., 2010; Vyas et al., 2011; Williamson, 2002). Withanolides are an active
ingredient that includes steroidal saponin, alkaloids, and steroidal lactones. Withaferin-A and
Withanolide D, as well as new Withanolide Glycosides Withanoside I–VII, contribute the
majority of biological action (Matsuda et al., 2001). Previous research has shown that certain
phytoconstituents from medicinal plants interact with SARS CoV-2 Mpro and other COVID-
19 target proteins (S, E, and N). These phytoconstituents include Withaferin A, Withanolide
B, Somniferine A, Withanolide, glucoside, and Withanone (Dharmendra & Deepak, 2020).

Ayurvedic formulations can play an important role in the production of healthy and nontoxic
therapeutic moieties. An attempt was made to identify new active and stable inhibitors
against novel coronavirus main protease using in silico molecular docking and molecular
dynamic simulation studies, from a total of 102 active phytoconstituents from a medicinal
plant. As a result, viral translation into functional polyproteins, which is necessary for virus
replication, is inhibited, and host physiological/biological functions are disrupted.

Lianhuaqingwen (LH):

Lianhuaqingwen (LH) is a patented Chinese medicine product that has been developed for
the treatment of cold and influenza. Nowadays it is widely used as an antiviral agent in
clinical practice, especially for various respiratory virus infections on a series of influenza
viruses by inhibiting viral replication and regulating immune function, and has achieved
similar therapeutic effectiveness with Oseltamivir in reducing the course of H1N1 virus
infection. Although LH significantly relieved the clinical symptoms of the COVID-19, the
underlying mechanism of antiviral effects on coronavirus, especially in the SARS-COV-2 is
by inhibiting virus replication and reducing the cytokine release from host cells.This is useful
in the therapeutic use of LH in combination with current drugs for the treatment of COVID-
19. However, the pharmaceutical components and pharmacological mechanism of LH in
fighting COVID-19 are still largely unexplored.

LH has the functions of clearing away heat and detoxifying the lungs, and thus it is also
clinically used to treat patients with the symptoms of fever and stagnation of the lung. In
comparison to oseltamivir, LH had a stronger effect on the relief of fever, cough, sore throat,
and fatigue in an anti-influenza A (H1N1) trial. Furthermore, it showed comparative
therapeutic effectiveness in the reduction of illness duration and viral shedding duration.

LH inhibits the spread of influenza viruses from different strains in vitro, with a 50%
inhibitory concentration (IC50) ranging from 0.35 to 2 mg/ml. It could also suppress the
virus-induced nuclear factor κB (NF-κB) activation and reduce the virus-induced gene
expression of interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor-α (TNF-α),
interferon-γ-inducible protein-10 (IP-10), and monocyte chemoattractant protein-1 (MCP-1).
Using a similar in vitro study, it has been shown that LH exerted anti-SARS-CoV-2 activity
by inhibiting virus replication and reducing cytokine release from host cells. by using
network pharmacology, it is found that there are 15 active components in LH and 61 related
targets. And the active components of LH might inhibit cytokine storms by regulating various
inflammatory signal pathways.

Lianhuaqingwen capsule has been confirmed to show therapeutic effects by clinical research
and observation. the course of treatment is from 7 to 10 days, indicating the effectiveness of
LH in treating COVID-19.
Conclusion:

Current findings and the recent knowledge about SARS-CoV and SARS-CoV-2 pathology,
profess the use of Ayurvedic Kadha in the prevention and management of COVID-19. The
phytochemicals found in the Kadha have a significant binding affinity with the different
CoVs proteins (Scheme 1), indicating that they may control viral infection and multiplication
in the host cells. Molecular docking study with human inflammatory mediators predicts that
many of the phytochemicals present in this preparation have significant anti-inflammatory
property. Most of the phytochemicals found in the herbs Ashwagandha, Giloy, Tulsi, Clove
and Black pepper have the potential to interact with most of the druggable proteins selected
in this study. In conclusion, regular consumption of ayurvedic Kadha in consultation with an
ayurvedic practitioner may decrease the inflammatory response, boost the individual’s
immunity and reduce the risk of CoVs infection including SARS-CoV-2.

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