SARS CoV-2 and COVID 19


A group of scientists are actively studying specific plants and terpenes to help humans cope with SARS CoV-2. This blog explores what we know so far about  how SARS enters the host cell and the body’s immune-response. The better we can understand the interaction between SARS CoV-2 and the host, the better we can explore the possibilities of the most effective terpenes for therapy.

SARS CoV-2 is a virus. The disease That the virus causes is known as COVID-19 (Corona Virus Disease). It shares approximately 76% genetic similarity to the SARS coronavirus.

Like other corona viruses such as versions of the cold, spike proteins radiate from the virus like a crown.

These spike proteins binds to the ACE2 (angiotensin converting enzyme) receptor in our cells. ACE2 receptors can be found in high amounts in Type II alveolar cells in the lungs. ACE2 receptors are also in the small intestine and colon, heart, kidneys, bladder, and the brain. This is possibly why there are such varied symptoms with SARS CoV-2; difficulty breathing, diarrhea, renal failure, and a loss of smell and taste.


In order for an infection to occur, the spike protein must bind to the ACE2 receptor. SARS CoV-2 does this by using the enzyme TMPRSS2 (Type II Transmembrane Serine Protease) to prime the spike S-protein into S1 & S2 subcomponents. The S1 component of the spike binds to the ACE2 receptor and the S2 component assists in fusing the viral membrane to the host cell.

Our lungs are composed of hundreds of millions of air sacs called alveoli. The alveoli have 2 types of cells to facilitate exchange of oxygen and carbon dioxide. Type 1 alveoli cells allow the oxygen to pass through the cell membrane, and Type 2 alveoli cells create a surfactant that coats the interior of the alveoli and prevent the cell wall from collapsing.


SARS CoV-2 attacks the type II alveoli cell. When infection begins, the body sends specialized cells called macrophages to the infection site. Macrophages produce cytokines which trigger inflammation and send signals for more macrophages. An over-reactive immune response of cytokines and inflammation is known as a ‘cytokine storm’ and can lead to fatalities.

As the infection advances, liquid begins to fill the alveoli leading to pneumonia. Impaired surfactant production from infected type II cells can lead to collapse of alveoli cells. In the above illustration, Acute Respiratory Distress Syndrome (ARDS) is level 6.

A comprehensive strategy for terpene therapy targets the following points in the infection cycle:

  1. Cytotoxicity: the use of essential oil, based hand sanitizers; room diffusers; and skin care products are part of prevention strategies. The following terpenes are highly anti-viral: 1, 8-cineole (eucalyptol), geraniol, carvacol, linalool, a-bisabolol, ocimene, pinene, pineol, thymoquinone, P-cymene, beta-caryophyllene
  1. Receptor Blocking: Utilizing terpenes which bind to the ACE2 receptor and prevent the virus from docking. There is a study determining the blocking capacity of garlic essential oil to the ACE2 protein (host receptor for SARS CoV-2). In addition, garlic essential oil also blocks the PDB6LU7 protein (main protease of SARS CoV-2). The high organosulfur compounds in garlic essential oil are believed to have strong interactions with the amino acids of the ACE2 protein.
  1. Serine Protease Inhibition: The enzyme TMPRSS2 is a Serine Protease, necessary for the virus to prime its spike protein as well as fuse to the cell membrane. Study identifies terpenes which are serine protease inhibitors. Viral inactivation has been discovered via inhibition by 1,8-cine ole (eucalyptol) of the main proteinase of SARS CoV-2, Mpro / 3CLpro.