Coronavirus as the name indicate, is virus in nature but it is truly virus in nature or bacteria ??This virus bacteria battle will resolve here.
Introduction :
In last days of December, china face large number of cases
presented with clinical symptoms of fever, dyspnea, dry cough and bilateral
lung filtrates on imaging. Causative agent of this pneumonia was found by
Chinese center for disease control and prevention (CCDC) through throat swab
samples and name as severe acute respiratory syndrome coronavirus-2
(SARS-coV-2). Later name was modified by WHO as COVID-19.
Their symptoms can be as mild from fever, dry cough and sore
throat to severe which are organ failure, pulmonary and severe edema with septic
shock which lead to Acute respiratory distress syndrome (ARDS).
Structure of coronavirus :
Coronavirus is envelope virus belong to Coronavirinae family, i.e. part of coronavidae family having single stranded ribonucleic acid (RNA). Its
structure is genomically resembles with coronavirus strains that was outbreak
in 2003.
Coronavirus have unique machinery
for replication and transcription, that work in RNA dependent RNA polymerase (RdRp) manner to replicate and transcript, key component of this machinery are nonstructural
proteins(nsps) which are formed by the cleavage of ORF1 and ORF1ab viral polyprotein.
Within non-structure proteins (nsps), nsp12 have main role in viral replication
and transcription along with nsp7 and nsp8 (work as co-factor),
So the primary targets for
anti-viral drug should be nsp12 to inhibit further viral replication and
transcription cascade.
Procoagulant-anticogulant balance
and corona bacteria misconception
Pathophysiology of coronavirus
same as other virus and bacteria that’s why it is misunderstood as
bacteria. Alike other bacteria when
virus invade in human it causes vascular permeability and multi organ
dysfunction and ultimately death by the
release of proinflammatory cytokines ( tumor necrotic factor, interleukin 6 and
interleukin 1β)
Due to the overproduction of cytokines, coagulation pathway
also activated , clot formed by the action of thrombin through the activation
of platelets and also covert fibrin into fibrinogen. PAR-1(proteinase
activating receptor) receptor have also major role in augmenting inflammation .
Thrombin which have major role in coagulation pathway
activated and clot formed, which is called thrombus. This can be inhibited or
reverse by natural physiological negative feedback mechanism which is anti thrombin
III, protein C system and tissue factor
pathway inhibitor. But in cytokine storm physiological anticoagulant and
coagulation pathway unbalanced due to the less production and more consumption
of physiological anticoagulation and that can ultimately lead to mutiorgan
dusfunction, secordanry to disseminated intravascular coagulation by forming
microthrombosis.
Evidence of disseminated intravascular coagulation found in non-survivors
COVID-19 patient with high d-dimers concentration.
Conculsion :
This pandemic virus is envelope virus that replicate
and transcript through RNA-dependent RNA polymerase manner that’s why it spread
everyday among thousand of peoples. We donot stuck only on its spreadibility
nature because due to the production of cytokine storm and defection in
physiological anticoagulant – coagulation pathway it lead to death by DIC .
DIC not only cause by bacteria but it also caused by virus
by the activation of thrombus and if its not controlled or balanced by natural
physiological pathway and through injectable anticoagulants i.e LMWH (low moleucular weight heparin) it
will worsen the condition as seen in non-survivors corona virus affected patient
it block the vessels through thrombus formatuion and lead to multiorgan
dtsfunction and death.
Targeting prophalylactic anticoagulation therapy will be
attractive for controlling the lethal effects like microthrombus and organ
dysfunction which ultimately give positive outcomes.
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