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* Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory cytokines.<ref name="pmid22390970">{{cite journal| author=Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG| title=Into the eye of the cytokine storm. | journal=Microbiol Mol Biol Rev | year= 2012 | volume= 76 | issue= 1 | pages= 16-32 | pmid=22390970 | doi=10.1128/MMBR.05015-11 | pmc=3294426 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22390970  }} </ref>
* During sepsis, cytokine storm may be the cause of cell or organ injury.<ref name="pmid28555385">{{cite journal| author=Chousterman BG, Swirski FK, Weber GF| title=Cytokine storm and sepsis disease pathogenesis. | journal=Semin Immunopathol | year= 2017 | volume= 39 | issue= 5 | pages= 517-528 | pmid=28555385 | doi=10.1007/s00281-017-0639-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28555385  }} </ref>


=== Cytokines ===
Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory [[Cytokine|cytokines]].<ref name="pmid22390970">{{cite journal| author=Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG| title=Into the eye of the cytokine storm. | journal=Microbiol Mol Biol Rev | year= 2012 | volume= 76 | issue= 1 | pages= 16-32 | pmid=22390970 | doi=10.1128/MMBR.05015-11 | pmc=3294426 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22390970  }} </ref>


* Cytokines are small proteins that are released for cell signaling.<ref name="pmid22390970" />
=== Cytokines Involved in Cytokine Storm ===
* Cytokine types and their actions include:<ref name="pmid22390970" />
 
** '''Interferons''' '''(INFs)'''
*[[Cytokine|Cytokines]] are small [[Protein|proteins]] that are released for [[cell signaling]].<ref name="pmid22390970" />
*** Key role in innate immunity  
*[[Cytokine|Cytokines]] types and their actions include:<ref name="pmid22390970" />
*** Regulation of the production of antiviral proteins
**'''Interferons''' '''(INFs)'''
*** Regulation of the production of antiproliferative proteins
*** Key role in [[Innate immune system|innate immunity]]
** '''Interleukins''' '''(ILs)'''
*** Regulation of the production of antiviral [[Protein|proteins]]
*** Regulation of immune cell differentiation and activation  
*** Regulation of the production of antiproliferative [[Protein|proteins]]
*** May be pro- or anti-inflammatory  
**'''Interleukins''' '''(ILs)'''
** '''Chemokines'''
*** Regulation of immune cell [[differentiation]] and activation  
*** May be pro- or anti-[[Inflammation|inflammatory]]  
**'''Chemokines'''
*** Act as chemoattractants
*** Act as chemoattractants
*** Recruitment of leukocytes
*** Recruitment of [[White blood cells|leukocytes]]
** '''Colony-stimulating factors'''  
**'''Colony-stimulating factors'''  
*** Induction of hematopoietic progenitor cell proliferation and differentiation  
*** Induction of [[Hematopoietic stem cell|hematopoietic progenitor cell]] [[Cell growth|proliferation]] and [[differentiation]]  
** '''Tumor necrosis factor (TNF)''' 
**'''Tumor necrosis factor (TNF)''' 
*** Activation of T cells (cytotoxic)
*** Activation of [[T cell|T cells]] ([[Cytotoxic T cell|cytotoxic]])


*  
*  
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*
*


=== Pathogenesis of ARDS by Cytokine Storm ===
=== Pathogenesis of Cytokine Storm ===


*In SARS coronavirus (SARS-CoV) and MERS coronavirus (MERS-CoV), cytokine storms have been associated with acute respiratory distress syndrome (ARDS).<ref name="pmid28466096">{{cite journal| author=Channappanavar R, Perlman S| title=Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. | journal=Semin Immunopathol | year= 2017 | volume= 39 | issue= 5 | pages= 529-539 | pmid=28466096 | doi=10.1007/s00281-017-0629-x | pmc=7079893 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28466096  }} </ref>
* Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory [[Cytokine|cytokines]].<ref name="pmid22390970" />
*In acute MERS-CoV infection, there is delayed release of cytokines and chemokines. However, later during the infection there is a rapid release of cytokines and chemokines.<ref name="pmid24077366">{{cite journal| author=Lau SKP, Lau CCY, Chan KH, Li CPY, Chen H, Jin DY | display-authors=etal| title=Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatment. | journal=J Gen Virol | year= 2013 | volume= 94 | issue= Pt 12 | pages= 2679-2690 | pmid=24077366 | doi=10.1099/vir.0.055533-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24077366  }} </ref>  
* During [[sepsis]], cytokine storm may be the cause of tissue or organ injury.<ref name="pmid28555385">{{cite journal| author=Chousterman BG, Swirski FK, Weber GF| title=Cytokine storm and sepsis disease pathogenesis. | journal=Semin Immunopathol | year= 2017 | volume= 39 | issue= 5 | pages= 517-528 | pmid=28555385 | doi=10.1007/s00281-017-0639-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28555385 }} </ref>
*Proinflammatory cytokines that have a role in ARDS include:<ref name="pmid15657466">{{cite journal| author=Jiang Y, Xu J, Zhou C, Wu Z, Zhong S, Liu J | display-authors=etal| title=Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome. | journal=Am J Respir Crit Care Med | year= 2005 | volume= 171 | issue= 8 | pages= 850-7 | pmid=15657466 | doi=10.1164/rccm.200407-857OC | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15657466  }} </ref><ref name="pmid17374415">{{cite journal| author=Cameron MJ, Bermejo-Martin JF, Danesh A, Muller MP, Kelvin DJ| title=Human immunopathogenesis of severe acute respiratory syndrome (SARS). | journal=Virus Res | year= 2008 | volume= 133 | issue= 1 | pages= 13-9 | pmid=17374415 | doi=10.1016/j.virusres.2007.02.014 | pmc=7114310 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17374415  }} </ref><ref name="pmid15655079">{{cite journal| author=Reghunathan R, Jayapal M, Hsu LY, Chng HH, Tai D, Leung BP | display-authors=etal| title=Expression profile of immune response genes in patients with Severe Acute Respiratory Syndrome. | journal=BMC Immunol | year= 2005 | volume= 6 | issue=  | pages= 2 | pmid=15655079 | doi=10.1186/1471-2172-6-2 | pmc=546205 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15655079 }} </ref><ref name="pmid32283152">{{cite journal| author=Ye Q, Wang B, Mao J| title=The pathogenesis and treatment of the `Cytokine Storm' in COVID-19. | journal=J Infect | year= 2020 | volume= 80 | issue= 6 | pages= 607-613 | pmid=32283152 | doi=10.1016/j.jinf.2020.03.037 | pmc=7194613 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32283152  }} </ref>
**IL-1β
**IL-6
**IL-8 (CXCL8)
**CCL-2 (MCP-1)
**CCL-3 (Macrophage inflammatory protein-1A)
**CCL-5
**IFNγ -induced protein10 (IP-10, CXCL10)
**Granulocytemacrophage colony-stimulating factor (GM-CSF)


* IFN-I or IFN-α/β play an important role in antiviral immune defense. 35,36
*Cytokine storm causes [[inflammation]], which in the beginning of the disease is [[local]] and later spreads around by the [[systemic circulation]]. This is followed by repair and restoration of tissues, [[Organ (anatomy)|organs]] and their functions. However, in severe or some [[Inflammation|inflammations]], the repair is with [[fibrosis]] which may lead to permanent dysfunction of organs.<ref name="pmid22390970" />
* which attract neutrophils and monocytes. This excessive infiltration of neutrophils and monocytes in the lung causes lung damage.
*Lung damage caused by pathogens (such as [[SARS-CoV]] and [[influenza virus]]) may lead to acute lung injury (ALI) or [[Acute respiratory distress syndrome|acute respiratory distress syndrome (ARDS)]].
**The IFN-α/β receptors on the surface of accumulated macrophages receive activating signals, this results in more production of chemokines by these cells which in turn results in further accumulation of macrophages. Therefore, more proinflammatory cytokines are produced and therefore the infection becomes more severe.
* [[Cytokine|Cytokines]] profiles change over time in patients with [[sepsis]]:<ref name="pmid22390970" />
**IFN-α/β or the proinflammatory cytokines produced by macrophages induce T-cell apoptosis, and this delays the antiviral immune defense process.
** In the early stages of the infection (minutes to hours),  [[Cytokine|cytokines]]  such as [[Tumor necrosis factors|TNF]] and [[IL-1]], and [[Chemokine|chemokines]] such as [[Interleukin 8|IL-8]] and [[CCL2|MCP-1 (CCL2)]] increase.
** Vascular leakage in the lungs and alveolar edema are caused by rapid cytokine increase that induce apoptosis in lung cells, which in turn results in hypoxia
** Then, an increase in [[Interleukin 6|IL-6]] is followed.
** Later, [[Interleukin 10|IL-10]] (anti-[[Inflammation|inflammatory]] cytokine) increases.


* Cytokines change over time in patients with sepsis:<ref name="pmid22390970" />
* Proinflammatory [[Cytokine|cytokines]] that have a role in [[Acute respiratory distress syndrome|ARDS]] include:<ref name="pmid15657466">{{cite journal| author=Jiang Y, Xu J, Zhou C, Wu Z, Zhong S, Liu J | display-authors=etal| title=Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome. | journal=Am J Respir Crit Care Med | year= 2005 | volume= 171 | issue= 8 | pages= 850-7 | pmid=15657466 | doi=10.1164/rccm.200407-857OC | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15657466  }} </ref><ref name="pmid17374415">{{cite journal| author=Cameron MJ, Bermejo-Martin JF, Danesh A, Muller MP, Kelvin DJ| title=Human immunopathogenesis of severe acute respiratory syndrome (SARS). | journal=Virus Res | year= 2008 | volume= 133 | issue= 1 | pages= 13-9 | pmid=17374415 | doi=10.1016/j.virusres.2007.02.014 | pmc=7114310 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17374415  }} </ref><ref name="pmid15655079">{{cite journal| author=Reghunathan R, Jayapal M, Hsu LY, Chng HH, Tai D, Leung BP | display-authors=etal| title=Expression profile of immune response genes in patients with Severe Acute Respiratory Syndrome. | journal=BMC Immunol | year= 2005 | volume= 6 | issue= | pages= 2 | pmid=15655079 | doi=10.1186/1471-2172-6-2 | pmc=546205 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15655079 }} </ref><ref name="pmid32283152">{{cite journal| author=Ye Q, Wang B, Mao J| title=The pathogenesis and treatment of the `Cytokine Storm' in COVID-19. | journal=J Infect | year= 2020 | volume= 80 | issue= 6 | pages= 607-613 | pmid=32283152 | doi=10.1016/j.jinf.2020.03.037 | pmc=7194613 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32283152  }} </ref>
** In the early stages of the infection (minutes to hours),  cytokines such as TNF and IL-1, and chemokines such as IL-8 and MCP-1 increase.
**IL-1β
** Increase in IL-6 is followed.
**[[Interleukin 6|IL-6]]
** Later, IL-10 (anti-inflammatory cytokine) increases.
**[[IL-8|IL-8 (CXCL8)]]
 
**[[CCL2|CCL-2 (MCP-1)]]
=== COVID-19 and Cytokine Storm ===
**[[CCL3|CCL-3 (Macrophage inflammatory protein-1A)]]
**[[CCL5|CCL-5]]
**IFNγ -induced protein 10 (IP-10, CXCL10)
**[[Granulocyte macrophage colony stimulating factor|Granulocytemacrophage colony-stimulating factor (GM-CSF)]]


===== Proinflammatory Cytokines =====
* Cytokine storm (dysregulated and excessive release of [[Cytokine|cytokines]]) has been associated with [[Acute respiratory distress syndrome|ARDS]] in [[SARS coronavirus|SARS coronavirus (SARS-CoV)]] and [[Middle East respiratory syndrome coronavirus infection causes|MERS coronavirus (MERS-CoV)]] infections.<ref name="pmid28466096">{{cite journal| author=Channappanavar R, Perlman S| title=Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. | journal=Semin Immunopathol | year= 2017 | volume= 39 | issue= 5 | pages= 529-539 | pmid=28466096 | doi=10.1007/s00281-017-0629-x | pmc=7079893 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28466096  }} </ref>
* <s>There have been reports on an association between cytokine storm and severity of [[COVID-19]] infection and COVID-19-associated-ARDS.</s>


* Significant increase in pro-inflammatory cytokines (such as IL-6), reduction in CD+8 T cells, suppressed Th1 antiviral responses and increase in IL-10 (a Th2 cytokine) have been reported to be associated with severe COVID-19 infection. (kupalli) Therefore, it has been suggested that  the pathogenesis of severe COVID-19 infection may be due to cytokine storm and suppressed Th1 antiviral responses. (kupalli)
*<s>Significant increase in pro-inflammatory [[Cytokine|cytokines]] (such as [[Interleukin 6|IL-6]]), reduction in [[Cytotoxic T cell|CD+8 T cells]], suppressed [[T helper cell|Th1]] antiviral responses and increase in [[Interleukin 10|IL-10]] (a [[T helper cell|Th2]] [[cytokine]]) have been reported to be associated with severe [[COVID-19]] infection. (kupalli) Therefore, it has been suggested that  the [[pathogenesis]] of severe [[COVID-19]] infection may be due to cytokine storm and suppressed [[T helper cell|Th1]] antiviral responses. (kupalli)</s>


* High levels of expression of IL-1B, IFN-γ , IP-10, and monocyte hemoattractant protein 1 (MCP-1) have been detected in patientswith COVID-19.  
*<s>High levels of expression of IL-1B, IFN-γ , IP-10, and [[CCL2|monocyte hemoattractant protein 1 (MCP-1)]] have been detected in patients with [[COVID-19]].  </s>
* These inflammatory cytokines may activate the Thelper type 1 (Th1) cell response.47 Th1 activation is a key event  in the activation of specific immunity.48
*<s>These inflammatory [[Cytokine|cytokines]] may activate the [[T helper cell|Thelper type 1 (Th1)]] cell response.47 [[T helper cell|Th1]] activation is a key event  in the activation of specific immunity.48</s>
* The serum levels of IL-2R and IL-6 in patients with COVID-19 are positively correlated with the severity  of the disease (i.e., critically ill patients > severely ill patients  > ordinary patients).49  
*<s>The serum levels of IL-2R and [[Interleukin 6|IL-6]] in patients with [[COVID-19]] are positively correlated with the severity  of the disease (i.e., critically ill patients > severely ill patients  > ordinary patients).49  </s>
* ther studies have found that, compared  with COVID-19 patients from general wards, patients in the intensive care unit (ICU) display increased serum levels of granulocyte  colony-stimulating factor, IP-10, MCP-1, macrophage inflammatory  protein-1A, and TNF-α. The above studies suggest that the cytokine  storm is positively correlated with disease severity.47  
*<s>ther studies have found that, compared  with [[COVID-19]] patients from general wards, patients in the [[Intensive care unit|intensive care unit (ICU)]] display increased serum levels of [[granulocyte  colony-stimulating factor]], IP-10, [[CCL2|MCP-1]], macrophage inflammatory  protein-1A, and [[Tumor necrosis factor-alpha|TNF-α]]. The above studies suggest that the cytokine  storm is positively correlated with disease severity.47</s>


===== Anti-inflammatory Cytokines =====
*<s>In contrast to [[Severe acute respiratory syndrome|SARS infection]], patients with [[COVID-19]] infection have high levels of  [[Interleukin 4|IL-4]] and [[Interleukin 10|IL-10]] (secreted  by [[Th2|Th2 cells]]), which are antiinflammatory [[Cytokine|cytokines]].</s>
 
* In contrast to SARS infection, patients with COVID-19 infection have high levels of  IL-4 and IL-10 (secreted  by Th2 cells), which are antiinflammatory cytokines.


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<br />
<s>Cytokine storm in the lung and systemic circulation causes acute lung injury (ALI) .(121) In the acute phase there is mononuclear and neutrophilic inflammatory response, followed by a chronic phase of fibroproliferation of collagen deposition in the lung tissue. (96)</s>


==<s>Overview</s>==
==<s>Overview</s>==

Revision as of 16:06, 11 July 2020

Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[1]


Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory cytokines.[1]

Cytokines Involved in Cytokine Storm

Pathogenesis of Cytokine Storm

  • Cytokine storm is an immune reaction that is characterized by dysregulated and excessive release of proinflammatory cytokines.[1]
  • During sepsis, cytokine storm may be the cause of tissue or organ injury.[2]
  • Significant increase in pro-inflammatory cytokines (such as IL-6), reduction in CD+8 T cells, suppressed Th1 antiviral responses and increase in IL-10 (a Th2 cytokine) have been reported to be associated with severe COVID-19 infection. (kupalli) Therefore, it has been suggested that the pathogenesis of severe COVID-19 infection may be due to cytokine storm and suppressed Th1 antiviral responses. (kupalli)
Cytokines Involved in COVID-19-Associated-Cytokine Storm
Proinflammatory Interferones
  • IFN-γ
Interleukines
  • IL-1β
  • IL-6
Chemokines
  • CCL-2 (MCP-1)
  • CCL-3 (Macrophage inflammatory protein-1A)
  • CCL-5
  • IL-8 (CXCL8)
  • IP-10 (CXCL10)
Colony-stimulating

factors  

  • GM-CSF
Tumor necrosis

factor  

  • TNF-α
Anti-inflammatory Interleukines
  • IL-4
  • IL-10




Overview

COVID-19-Associated Hematologic Findings

Pathophysiology and Causes

Epidemiology

  • Leukocytosis is seen in 11.4% of patients with severe COVID-19 infection compared to 4.8% of patients with non-severe infection.[10][11]
  • Increase in CRP is seen in 81.5% of patients with severe COVID-19 infection compared to 56.4% of patients with non-severe infection.[10][11]
  • Increase in procalcitonin is seen in 13.7% of patients with severe COVID-19 infection compared to 3.7% of patients with non-severe infection.[10][11]
  • Increase in AST is seen in 39.4% of patients with severe COVID-19 infection compared to 18.2% of patients with non-severe infection.[10][11]
  • Increase in ALT is seen in 28.1% of patients with severe COVID-19 infection compared to 19.8% of patients with non-severe infection.[10][11]
  • Increase in LDH is seen in 58.1% of patients with severe COVID-19 infection compared to 37.2% of patients with non-severe infection.[10][11]
  • MDW was found to be increased in all patients with COVID-19 infection, particularly in those with the worst conditions.[11]
  • Increase in total bilirubin is seen in 13.3% of patients with severe COVID-19 infection compared to 9.9% of patients with non-severe infection.[10][11]
  • Increase in creatinine is seen in 4.3% of patients with severe COVID-19 infection compared to 1% of patients with non-severe infection.[10][11]
  • Thrombocytosis has been reported in 4% of patients with COVID-19 infection.[12]

Clinical Significance

Laboratory findings in COVID-19 infection may indicate clinical abnormalities, including:

  • In patients with COVID-19 infection, leukocytosis may be an indication of a bacterial infection or superinfection.[11]
  • In patients with COVID-19 infection, increase in CRP may be an indication of severe viral infection or sepsis and viremia.[11]
  • In patients with COVID-19 infection, increase in procalcitonin may be an indication of bacterial infection or superinfection.[11]
  • There have been different reports regarding the association of increase in ferritin with death in COVID-19 infection; for example, there has been a report that increase in ferritin is associated with acute respiratory distress syndrome (ARDS) but not death[13], while another one reports an association between increase in ferritin and death in COVID-19 infection[14]
  • In patients with COVID-19 infection, increase in aminotransferases may indicate injury to the liver or multi-system damage.[11]
  • In patients with COVID-19 infection, increase in aminotransferases may indicate injury to the liver or multi-system damage.[11]
  • In patients with COVID-19 infection, increase in LDH may indicate injury to the lungs or multi-system damage.[11]
  • In patients with COVID-19 infection, increase in total bilirubin may indicate injury to the liver.[11]
  • In patients with COVID-19 infection, increase in creatinine may indicate injury to the kidneys.[11]
  • In patients with COVID-19 infection, increase in cardiac troponins may indicate cardiac injury.[11]
  • In patients with COVID-19 infection, decrease in albumin may indicate liver function abnormality.[11]
  • Increase in IL-6 has been reported to be associated with death in COVID-19 infection.[13]


References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Tisoncik JR, Korth MJ, Simmons CP, Farrar J, Martin TR, Katze MG (2012). "Into the eye of the cytokine storm". Microbiol Mol Biol Rev. 76 (1): 16–32. doi:10.1128/MMBR.05015-11. PMC 3294426. PMID 22390970.
  2. ↑ Chousterman BG, Swirski FK, Weber GF (2017). "Cytokine storm and sepsis disease pathogenesis". Semin Immunopathol. 39 (5): 517–528. doi:10.1007/s00281-017-0639-8. PMID 28555385.
  3. ↑ Jiang Y, Xu J, Zhou C, Wu Z, Zhong S, Liu J; et al. (2005). "Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome". Am J Respir Crit Care Med. 171 (8): 850–7. doi:10.1164/rccm.200407-857OC. PMID 15657466.
  4. ↑ Cameron MJ, Bermejo-Martin JF, Danesh A, Muller MP, Kelvin DJ (2008). "Human immunopathogenesis of severe acute respiratory syndrome (SARS)". Virus Res. 133 (1): 13–9. doi:10.1016/j.virusres.2007.02.014. PMC 7114310 Check |pmc= value (help). PMID 17374415.
  5. ↑ Reghunathan R, Jayapal M, Hsu LY, Chng HH, Tai D, Leung BP; et al. (2005). "Expression profile of immune response genes in patients with Severe Acute Respiratory Syndrome". BMC Immunol. 6: 2. doi:10.1186/1471-2172-6-2. PMC 546205. PMID 15655079.
  6. ↑ Ye Q, Wang B, Mao J (2020). "The pathogenesis and treatment of the `Cytokine Storm' in COVID-19". J Infect. 80 (6): 607–613. doi:10.1016/j.jinf.2020.03.037. PMC 7194613 Check |pmc= value (help). PMID 32283152 Check |pmid= value (help).
  7. ↑ Channappanavar R, Perlman S (2017). "Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology". Semin Immunopathol. 39 (5): 529–539. doi:10.1007/s00281-017-0629-x. PMC 7079893 Check |pmc= value (help). PMID 28466096.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 Frater JL, Zini G, d'Onofrio G, Rogers HJ (2020). "COVID-19 and the clinical hematology laboratory". Int J Lab Hematol. 42 Suppl 1: 11–18. doi:10.1111/ijlh.13229. PMC 7264622 Check |pmc= value (help). PMID 32311826 Check |pmid= value (help).
  9. ↑ Meisner M (2014). "Update on procalcitonin measurements". Ann Lab Med. 34 (4): 263–73. doi:10.3343/alm.2014.34.4.263. PMC 4071182. PMID 24982830.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7
  11. ↑ 11.00 11.01 11.02 11.03 11.04 11.05 11.06 11.07 11.08 11.09 11.10 11.11 11.12 11.13 11.14 11.15 11.16 11.17 11.18 Lippi G, Plebani M (2020). "The critical role of laboratory medicine during coronavirus disease 2019 (COVID-19) and other viral outbreaks". Clin Chem Lab Med. 58 (7): 1063–1069. doi:10.1515/cclm-2020-0240. PMID 32191623 Check |pmid= value (help).
  12. ↑ Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y; et al. (2020). "Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study". Lancet. 395 (10223): 507–513. doi:10.1016/S0140-6736(20)30211-7. PMC 7135076 Check |pmc= value (help). PMID 32007143 Check |pmid= value (help).
  13. ↑ 13.0 13.1 Wu C, Chen X, Cai Y, Xia J, Zhou X, Xu S; et al. (2020). "Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China". JAMA Intern Med. doi:10.1001/jamainternmed.2020.0994. PMC 7070509 Check |pmc= value (help). PMID 32167524 Check |pmid= value (help).
  14. ↑ Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z; et al. (2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. PMC 7270627 Check |pmc= value (help). PMID 32171076 Check |pmid= value (help).


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