Brief Introduction of COVID19, detailed procedure of COVID19 Infection, and available treatments options.

1. Introduction,
Pathophysiology, and
Treatment Options for
COVID-19
Ahmed Madni
PhD Scholar
Nanobiotechnology Group, Industrial Biotechnology
Division, National Institute for Biotechnology and
Genetic Engineering (NIBGE), Faisalabad

2. List of Contents
• Brief Introduction
• Symptoms
• Cellular Targets
• COVID-19 and Autoimmune System
• Current Treatments
• Status of Pakistan
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3. COVID-19 (Phenotypic and Genomic Organization)
Ref: The Novel Insight of SARS-CoV-2 Molecular Biology and Pathogenesis and Therapeutic Options
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COVID-19 consists of a single, positive-stranded RNA that is 29,811 nucleotides long

4. Ref: Epidemiology of Novel Corona Virus (Covid-19): A Review
COVID-19 Phylogenetic Tree
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5. COVID-19 Evolutionary Event
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6. COVID-19 Phylogenetic Tree
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7. Common Symptoms in COVID-19 Patients
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8. Ref: COVID-19 pathophysiology: A review
Severity in Symptoms of COVID-19 Patients
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9. • The variants have different origins but share a mutation in a gene that
encodes the spike protein, which the virus uses to latch on to and enter
human cells
• The problem is, the more variants we get, the greater the chance the virus
will be able to escape part of the vaccine - and this may reduce [its]
efficacy
How COVID-19 Variations are Evolving Efficiently
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10. • The novel coronavirus SARS-CoV-2 entry into host cells is mediated by its
spike glycoprotein (S-glycoprotein), and the angiotensin-converting
enzyme 2 (ACE2) has been identified as a cellular receptor
Cellular Targets of COVID-19
Ref: Molecular interaction and inhibition of SARS-CoV-2 binding to the ACE2 receptor
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11. • ACE2 is present in many cell types and tissues including the lungs,
heart, blood vessels, kidneys, liver and gastrointestinal tract.
• ACE2 is present in epithelium in the nose, mouth and lungs. In the
lungs, ACE2 is highly abundant on type 2 pneumocytes, an important
cell type present in chambers within the lung called alveoli, where
oxygen is absorbed and waste carbon dioxide is released.
Cellular Targets of COVID-19
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12. 12
The ACE enzyme converts angiotensin I (ANG I) into angiotensin II (ANG II).
The main role of ACE2 is to break down ANG II into molecules that
counteract angiotensin II’s harmful effects; but if the virus occupies the
ACE2 ‘receptor’ on the surface of cells, then its role is blunted (red lines).
Drugs called ACE inhibitors inhibit the formation of ANG II, which would
otherwise interact with the angiotensin type 1 receptor to produce tissue
damage and inflammation. Drugs called ARBs block angiotensin II from
interacting with its receptor. ANG II drives lung injury. If there is a decrease
in ACE2 activity (because the virus is binding to it), then ACE2 can’t
break down the ANG II protein, which means there is more of it to cause
inflammation and damage in the body (abnormally high ANG II activity)
Angiotensin-converting Enzyme 2 (ACE2)

13. • Angiotensin converting enzyme (ACE, aka ACE1) is another protein, also found in tissues such as the lung and heart,
where ACE2 is present. Drugs that inhibit the actions of ACE1 are called ACE inhibitors. Examples of these drugs are
ramipril, lisinopril, and enalapril.
• These drugs block the actions of ACE1 but not ACE2. ACE1 drives the production of ANG II. In effect, ACE1 and
ACE2 have a “yin-yang” relationship; ACE1 increases the amount of ANG II, whereas ACE2 reduces ANG II.
• By inhibiting ACE1, ACE inhibitors reduce the levels of ANG II and its ability to increase blood pressure and tissue
injury. ACE inhibitors are commonly prescribed for patients with hypertension, heart failure and kidney disease.
• Another commonly prescribed class of drugs, angiotensin receptor blockers (ARBs, e.g., losartan, valsartan, etc.) have
similar effects to ACE inhibitors and may also be useful in treating COVID-19.
Ref: https://theconversation.com/what-is-the-ace2-receptor-how-is-it-connected-to-coronavirus-and-why-might-it-be-
key-to-treating-covid-19-the-experts-explain-136928
What are ACE inhibitors? Are they a possible treatment or
prophylactic for SARS-CoV-2?
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14. Ref: Epidemiology of Novel Corona Virus (Covid-19): A Review
Cellular Entrance and Replication
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15. • The body produces “autoantibodies”, these are antibodies that – instead of attacking the
invading virus – attack the patient’s own immune system and organs
• Excess Cytokines and Chemokines – important messengers in the immune system, this
interferes with the normal immune system function, blocking antiviral defenses,
potentially making the disease more severe
• People with severe COVID can also develop autoantibodies to interferons, immune
proteins that play a major role in fighting viral infections.
Ref: https://theconversation.com/severe-covid-may-be-caused-by-autoantibodies-here-is-what-that-means-152053
COVID-19 and Autoimmune Response
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16. COVID-19 and Autoimmune Response
Ref: Nature and functions of autoantibodies
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17. • In addition, there are a number of similarities between the amino acid sequences of [coronavirus]
proteins and those of human proteins
• These protein similarities may confuse the immune system and cause it to attack its own healthy cells; in
some people, this attack may continue even after the true virus cells have been wiped out
• Autoimmunity could explain why a robust immune response to the virus — one that includes the
production of coronavirus-neutralizing antibodies — does not always correlate with mild Covid-19. It
may be that in some patients, an immune response intended to eliminate the virus ends up also attacking
healthy cells
• These autoimmune phenomena could also explain why myocarditis and other forms of inflammation or
injury show up weeks or months after a person has ostensibly recovered from a coronavirus infection
Ref: COVID-19: Infection or Autoimmunity
COVID-19 and Autoimmune Response
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18. • Firstly, the expression level of ACE2 may differ between adults and
children. A previous study showed that ACE2 was more abundantly
expressed on well-differentiated ciliated epithelial cells. Human lung and
epithelial cells continue to develop following the birth. ACE2 expression
may be lower in pediatric population.
• Secondly, with ageing, continuous antigen stimulation and thymic
involution lead to a shift in T cell subset distribution from naïve T cells to
central memory T cells, effector T cells and effector memory T cells. This
process is accompanied by the loss of expression of co-stimulatory
molecules such as CD27 and CD28, with increased susceptibility to
infections
Infant Vs Aged Group Infection against COVID-19
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19. Ref: https://www.worldometers.info/coronavirus/
Cases Till-date
Total cases comprise worldwide
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20. Treatments via Vaccine
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21. In-trials Vaccine
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22. Ref: https://www.bbc.com/news/world-asia-china-55498197
Most Effective Vaccines
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23. What About Vaccine Update in Pakistan?
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24. Alternative of Treatments
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25. Thank you!