Dynamics of Induced Hyper-inflammatory States in Essential Replication- Induced Host Cell Injury in Acute Respiratory Distress Syndrome As Covid 19 Reformulation of Vesicle Genesis in Pneumocyte Type Ii Cells

Lawrence M. Agius

FORMERLY OF Department of Pathology, Mater Dei Hospital, Tal-Qroqq, University of Malta Medical School Msida, Malta

CitationCitation COPIED

Agius LM. Dynamics of Induced Hyper-inflammatory States in Essential Replication- Induced Host Cell Injury in Acute Respiratory Distress Syndrome As Covid 19 Reformulation of Vesicle Genesis in Pneumocyte Type Ii Cells. 2020 Jun;2(1):106.


Hyper inflammation constitutes dimensions of non-resolution in the induction of dynamic transcription and translation of actively replicating COVID 19 viral particles as specifically restricted by the ACE2 receptor and as further induction of vesicle genesis of the lipid bilayer of the host cell plasma membrane. The actual process of inclusion of the nucleocapsid and the nature of such inclusion in bilayer biology is a distinctive reformulation of the active transfer of evolutionary consequence as dictated by inflammasome instability. The particular dimensions of actuation of the cellular injury is paramount consideration in a viral biology that transmits the formulation of injury as conversion dynamics of promoted dimensions in replication and transmission of the COVID 19 viral particles.


The byproducts of transcribed and actively replicating COVID 19 viral particles constitute a range of cytokines and chemokines that strongly provoke a hyper storm inflammatory state that specifically targets the type II pneumocytes in the alveolar membranes and the various regions of the terminal broncho alveolar cell type derivatives. Understanding the pathophysiology and immunobiology underlying the clinical features of COVID-19 infection is essential to for effective therapy [1]. In such terms, an exquisite targeting phenomenon is directed towards cells that highly constitute expression of the angiotensin converting enzyme protein 2 (ACE2) on the host plasma membrane. The hyper inflammatory response is responsible for disease severity and death in infected individuals [2]. An interplay between coagulation and inflammation essentially constitute the microenvironmental conditioning of the viral infection [3,4]. Essential priming of the spike surface protein by TMPRSS2 serine proteases is followed by fusion with the lipid bilayer of the host cells and the entry of the viral particles as included within vesicles. The release of virus particles within the host cell cytoplasm is followed by directed distribution to the endoplasmic reticulum and Golgi apparatus to further the release of nucleoprotein capsid structural components.

Turnover Dynamics

Dynamics of turnover of virus particles are somehow coordinated with distribution and release of the COVID 19 particles in a manner that comprises infectivity activities that are linked to marked inflammatory responses in the regions rich in viral particles. Vitamin D supplementation could reduce of COVID-19 infections [5]. The replication of COVID 19 is a consequence of transcription within cellular cytoplasm as strictly dictated by the fusion of the spike membrane protein originally targeting the host membrane bilipid component of the plasma membrane. The binding of COVID-19 to the Toll like receptor induces the release of pro-IL-1beta with inflammasome action and the release of active mature IL-1beta [6].

As such, the evolutionary course of the COVID 19 is subtotally derived from the genomic organization and reorganization of the SARS CoV that provoked 8000 infected cases and 800 deaths in 2002 2003 acute respiratory distress syndrome. Cardiovascular complications induce myocarditis, acute myocardial infarction, heart failure, venous thrombosis and arrhythmias [7,8].

Pandemic Reformulation

The derivative dimensions of the 2019 pandemic are hence consequential result of an essential evolutionary series of changes within an essential setting of preservation of subtotal genomic integrity and of nonstructural protein apparatus. A dysregulated macrophage response can induce pathologic lesions as in the related virus SARS-CoV [9]. In such terms, the further conformational derivation from SARS CoV original species of virus is hence an adaptive re-confrontation within system of consequential sequence reconfirmation with highly restricted evolutionary adaptability. The experiences encountered in the previous SARS and MERS vaccine research may be utilised in the development of COVID-19 [10].

Dimensions of cooperative submission constitute a realization of injury to the host cell plasma membrane with the added connotation of such injury within encompassed formulation as directed by genesis of distributing vesicle genesis. It is to be noted that evolutionary dynamics are defining terms in the redistribution of active genesis of vesicles as specifically constituted by the host cell lipid bilayer of the external plasma membrane and as further formulated by the angiotensin converting enzyme receptor 2.

Constitutive and Reconstitutive Attributes

Thus, constitutive attributes of the host cells as these interact with restricted evolutionary dynamics of the COVID 19 are directed to a marked pro-inflammatory series of activities that actively participate with the resultant instability of the inflammasome in the host cell cytoplasm. In such terms, derivative phenomena of consequence are earmark biologic dimensions of a host cell that is active participant in redistribution of replicating viral particles. Decreased T cell populations contribute to the progressive severity of COVID-19 [11]. Consequential inclusion dynamics of such redistribution appear to involve in terms of implied result the further adaptability of the COVID 19 particles to such hyper inflammatory states. Hence, the revolutionary but restricted evolutionary course of the COVID 19 is a mechanism that promotes and self-promotes evolutionary consequences of such hyper inflammation as terms of progression of the host cells in particular [12]. The successful virus isolation attempts have enhanced the development of better diagnostics and effective vaccines [13].

The further inclusive derivation of such injury to cells and to the alveolar membranes in particular are consequences to establishment towards exquisite targeting of the type II pneumocytes in a process of both pulmonary edema generation and of hyaline membrane deposition. In such contextual derivation, the resetting of the inflammasome activities are basic formulation for the replication of transcribed viral particles within strictly confined redistribution within the host cell cytoplasm as initial dynamics of the transcription of such viral particles. Inclusive performance of genesis of proinflammatory states are central players within consequential redistribution of the COVID 19 particles as dictated by vesicle genesis in the first instance. Autophagy is involved in the antiviral response at multiple levels, including firophagy, the presentation of viral antigens, the status fitness of immune cells and the suppression of excessive inflammation [14].

Lipid Bilayer of Host Cells

Lipid bilayer inclusion of the viral nucleocapsid as biology of the ACE receptor dynamics comprises and inclusive phenomenon of plasma membrane reconstitution linked intimately to the inflammatory storm genesis as further evidenced also by extra pulmonary redistribution of the COVID 19 particles.

It is further to such considerations that predominant cascade events are increased momentum genesis of cytokines and chemokines that promote in real terms the re-characterized consequences of infectivity and transmissibility of injury states within the primary component derivatives of an acute respiratory distress phenomenon. It is hence consequential recharacterization of such hyper inflammation that the pathobiology of the COVID 19 infection both provokes and further modulates the increasingly effective transcription and translation of replicating viral particles. On the basis of current studies, it is perhaps the combined antiviral treatment which has shown the highest success rate [15].

Concluding Remarks

Derivative phenomena of consequence of hyper inflammation storms are participant players in redistribution of a COVID 19 that is specifically and constitutively restricted in terms of genesis of inclusive vesicles but which is supported in active biology of redistribution of the viral particles. A central enigmatic dynamics would implicate the host parent cell in remodulation of the essential shifting progression from proinflammatory states to a hyper inflammatory storm borne out by cytokine and chemokine cascades of evolution from the dynamic range of evolutionary progression to the COVID 19 biologic states.

Provocative induction phenomena are hence defining terms in the realization of an injury that is recharacterized as pneumocyte type II reformulation and as specifically provoked by the hyper inflammation of derivative and genesis attributes of promoted constitution and derivation. The phenomenon of consequential derivation is a paramount consideration of a generic series of constitutional membrane biologic profile that cooperates as derived dynamics of fusion of the spike surface protein of the COVID 19 and of the ACE2 receptor in reformulated genesis and redistribution of vesicle genesis and biology


  1. Zirui Tay M, Poh CM, Renia L, MacAry PA, Ng LP. The trinity ofCOVID-19: immunity, inflammation and intervention Nat RevImmunol. 2020 Jun;20(6):363-374. 
  2. Merad M, Martin JC. Pathological inflammation in patients withCOVID-19: A key role for monocytes and macrophages Nat RevImmune. 2020 Jun;1-8. 
  3. Kowalewski M, Fina D, Slomka A, Raffa GM, Martucci G, Coco VL,et al. COVID-19 and ECMO: the interplay between coagulationand inflammation-a narrative review Crit Care. 2020;24(1):205. 
  4. Jose RJ, Manuel A. COVID-19 cytokine storm: the interplaybetween inflammation and coagulation. Lancet Respir Med. 2020Apr;S2213-2600. 
  5. Grant WB, Lahore H, McDonnell SL, Beggarly CA, French CB, etal. Evidence that vitamin D supplementation could reduce riskof influenza and COVID-19 infections and death Nutrients. 2020Apr;12(4):E988. 
  6. Conti P, Ronconi G, Caraffa A, Galena C, Ross R, et al. Inductionof pro-inflammatory cytokines (IL-1 and IL-6) and lunginflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2):anti-inflammatory strategies J Biol Regul Homeost Agents. 2020Mar;34(2):1. 
  7. Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascularcomplications in COVID-19. Am J Emerg Med. 2020Apr;S0735-6757. 
  8. Akhmerov A, Marban E. COVID-19 and the heart. Circ Res. 2020May;126(10):1443-1455. 
  9. Merad M, Martin JC. Pathological inflammation in patients withCOVID-19: a key role for monocytes and macrophages. Nat RevImmunol. 2020 Jun;1-8
  10. Yang L, Tian D, Liu W. Strategies for vaccine developmentof COVID-19 SHENG WU GONG CHENG XUE BAO. 2020Apr;36(4):593-604. 
  11. 11. Liu R, Wang Y, Li J, Han H, Xia Z, Liu F, et al. Decreased T cellpopulations contribute to the increased severity of COVID
  12. Habibzadeh P, Stonemason EK. The novel coronavirus: a bird’seye view. Int J Occup Environ Med. 2020 Apr;11(2):65-71. 
  13. Malik YS, Sirdar S, Bhat S, Sharun K, Dhama K, et al. Emergingnovel coronavirus (2019-nCoV)—current scenario, evolutionaryperspective based on genome analysis and recent developments.Vet Q. 2020 Dec;40(1):68-76.
  14. Carmona-Gutierrez D, Bauer MA, Zimmermann A, Kainz K, HoferSJ, et al. Digesting the crisis: autophagy and coronaviruses MicrobCell. 2020 Dec;7(5):119-128. 
  15. Yan Y, Shin W, Pang YX, Meng Y, Lai J, et al. The first 75 days ofnovel coronavirus (SARS-CoV-2) outbreak: recent advances,prevention, and treatment Int J Environ Res Public Health. 2020Mar;17(7):2323.