COVID-19 – Considerations for the paediatric rheumatologist
Identifieur interne : 001717 ( Pmc/Corpus ); précédent : 001716; suivant : 001718COVID-19 – Considerations for the paediatric rheumatologist
Auteurs : Christian M. HedrichSource :
- Clinical Immunology (Orlando, Fla.) [ 1521-6616 ] ; 2020.
Abstract
The novel coronavirus SARS-CoV2 is a threat to the health and well-being of millions of lifes across the globe. A significant proportion of adult patients require hospitalisation and may develop severe life-threatening complications. Children, on the other hand, can carry and transmit the virus, but usually do not develop severe disease. Mortality in the paediatric age-group is relatively low. Differences in virus containment and clearance, as well as reduced inflammation-related tissue and organ damage may be caused by age-specific environmental and host factors. Since severe complications in adults are frequently caused by uncontrolled immune responses and a resulting “cytokine storm” that may be controlled by targeted blockade of cytokines, previously established treatment with immunosuppressive treatments may indeed protect children from complications.
Url:
DOI: 10.1016/j.clim.2020.108420
PubMed: 32283324
PubMed Central: 7151358
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">COVID-19 – Considerations for the paediatric rheumatologist</title><author><name sortKey="Hedrich, Christian M" sort="Hedrich, Christian M" uniqKey="Hedrich C" first="Christian M." last="Hedrich">Christian M. Hedrich</name><affiliation><nlm:aff id="af0005">Department of Women's & Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK</nlm:aff></affiliation><affiliation><nlm:aff id="af0010">Department of Paediatric Rheumatology, Alder Hey Children's NHS Foundation Trust Hospital, Liverpool, UK</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32283324</idno><idno type="pmc">7151358</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151358</idno><idno type="RBID">PMC:7151358</idno><idno type="doi">10.1016/j.clim.2020.108420</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">001717</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001717</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">COVID-19 – Considerations for the paediatric rheumatologist</title><author><name sortKey="Hedrich, Christian M" sort="Hedrich, Christian M" uniqKey="Hedrich C" first="Christian M." last="Hedrich">Christian M. Hedrich</name><affiliation><nlm:aff id="af0005">Department of Women's & Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK</nlm:aff></affiliation><affiliation><nlm:aff id="af0010">Department of Paediatric Rheumatology, Alder Hey Children's NHS Foundation Trust Hospital, Liverpool, UK</nlm:aff></affiliation></author></analytic><series><title level="j">Clinical Immunology (Orlando, Fla.)</title><idno type="ISSN">1521-6616</idno><idno type="eISSN">1521-7035</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The novel coronavirus SARS-CoV2 is a threat to the health and well-being of millions of lifes across the globe. A significant proportion of adult patients require hospitalisation and may develop severe life-threatening complications. Children, on the other hand, can carry and transmit the virus, but usually do not develop severe disease. Mortality in the paediatric age-group is relatively low. Differences in virus containment and clearance, as well as reduced inflammation-related tissue and organ damage may be caused by age-specific environmental and host factors. Since severe complications in adults are frequently caused by uncontrolled immune responses and a resulting “cytokine storm” that may be controlled by targeted blockade of cytokines, previously established treatment with immunosuppressive treatments may indeed protect children from complications.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Zhu, N" uniqKey="Zhu N">N. Zhu</name></author><author><name sortKey="Zhang, D" uniqKey="Zhang D">D. Zhang</name></author><author><name sortKey="Wang, W" uniqKey="Wang W">W. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Immunol</journal-id><journal-id journal-id-type="iso-abbrev">Clin. Immunol</journal-id><journal-title-group><journal-title>Clinical Immunology (Orlando, Fla.)</journal-title></journal-title-group><issn pub-type="ppub">1521-6616</issn><issn pub-type="epub">1521-7035</issn><publisher><publisher-name>Published by Elsevier Inc.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32283324</article-id><article-id pub-id-type="pmc">7151358</article-id><article-id pub-id-type="publisher-id">S1521-6616(20)30259-X</article-id><article-id pub-id-type="doi">10.1016/j.clim.2020.108420</article-id><article-id pub-id-type="publisher-id">108420</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>COVID-19 – Considerations for the paediatric rheumatologist</article-title></title-group><contrib-group><contrib contrib-type="author" id="au0005"><name><surname>Hedrich</surname><given-names>Christian M.</given-names></name><email>E.christian.hedrich@liverpool.ac.uk</email><xref rid="af0005" ref-type="aff">a</xref><xref rid="af0010" ref-type="aff">b</xref><xref rid="cr0005" ref-type="corresp">⁎</xref></contrib></contrib-group><aff id="af0005"><label>a</label>Department of Women's & Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK</aff><aff id="af0010"><label>b</label>Department of Paediatric Rheumatology, Alder Hey Children's NHS Foundation Trust Hospital, Liverpool, UK</aff><author-notes><corresp id="cr0005"><label>⁎</label>Corresponding author at: Institute in the Park, Alder Hey Children's NHS Foundation Trust Hospital, East Prescot Road, Liverpool L14 5AB, UK. <email>E.christian.hedrich@liverpool.ac.uk</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>10</day><month>4</month><year>2020</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="epub"><day>10</day><month>4</month><year>2020</year></pub-date><elocation-id>108420</elocation-id><history><date date-type="received"><day>9</day><month>4</month><year>2020</year></date></history><permissions><copyright-statement>© 2020 Published by Elsevier Inc.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder></copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions><abstract id="ab0005"><p>The novel coronavirus SARS-CoV2 is a threat to the health and well-being of millions of lifes across the globe. A significant proportion of adult patients require hospitalisation and may develop severe life-threatening complications. Children, on the other hand, can carry and transmit the virus, but usually do not develop severe disease. Mortality in the paediatric age-group is relatively low. Differences in virus containment and clearance, as well as reduced inflammation-related tissue and organ damage may be caused by age-specific environmental and host factors. Since severe complications in adults are frequently caused by uncontrolled immune responses and a resulting “cytokine storm” that may be controlled by targeted blockade of cytokines, previously established treatment with immunosuppressive treatments may indeed protect children from complications.</p></abstract><abstract abstract-type="author-highlights" id="ab0010"><title>Highlights</title><p><list list-type="simple" id="l0005"><list-item id="li0005"><label>•</label><p id="p0005">The novel coronavirus SARS-CoV2 causes COVID-19, a pandemic threatening millions of lifes globally.</p></list-item><list-item id="li0010"><label>•</label><p id="p0010">Children with COVID-19 rarely develop severe symptoms and mortality is relatively low.</p></list-item><list-item id="li0015"><label>•</label><p id="p0015">Co-infections (and co-clearance) with other viruses may help children to overcome SARS-CoV2.</p></list-item><list-item id="li0020"><label>•</label><p id="p0020">Fewer comorbidities and age-specific host factors may protect children.</p></list-item><list-item id="li0025"><label>•</label><p id="p0025">Limited experience suggests that pre-existing anti-inflammatory treatment may not increase risk significantly.</p></list-item></list></p></abstract><kwd-group id="ks0005"><title>Keywords</title><kwd>COVID</kwd><kwd>SARS</kwd><kwd>SARS-CoV2</kwd><kwd>Paediatric</kwd><kwd>Inflammation</kwd><kwd>ARDS</kwd><kwd>Cytokine storm</kwd><kwd>Rheumatology</kwd></kwd-group></article-meta></front><body><sec id="s0005"><label>1</label><title>Mini review</title><p id="p0030">SARS-CoV2 is the pathogen causing COVID-19, a pandemic threatening millions of lifes globally. While in most individuals SARS-CoV2 infections are unapparent or associated with mild to moderate symptoms, as many as 10–20% develop severe or life-threatening disease [<xref rid="bb0005" ref-type="bibr">1</xref>].</p><p id="p0035">Surprisingly for an air-borne viral infection, the number for children diagnosed with COVID-19 is relatively small (2.1% of 42.672 confirmed COVID-19 cases in China were children and young people (<19 years)), and disease-associated mortality among children is low [<xref rid="bb0010" ref-type="bibr">2</xref>,<xref rid="bb0015" ref-type="bibr">3</xref>] (<xref rid="t0005" ref-type="table">Table 1</xref>).<table-wrap position="float" id="t0005"><label>Table 1</label><caption><p>Disease severity and laboratory findings in children with COVID-19.</p></caption><alt-text id="al0005">Table 1</alt-text><table frame="hsides" rules="groups"><thead><tr><th rowspan="2"><bold>Source</bold></th><th><bold>Cai <italic>et a.</italic></bold><hr></hr></th><th><bold>Cai et al.</bold><hr></hr></th><th><bold>Chen et al.</bold><hr></hr></th><th><bold>Feng et al.</bold><hr></hr></th><th><bold>Wang et al.</bold><hr></hr></th><th><bold>Zeng et al.</bold><hr></hr></th><th><bold>Zhang et al.</bold><hr></hr></th><th><bold>Liu et al.</bold><hr></hr></th><th><bold>Kam et al.</bold><hr></hr></th><th><bold>Chan et al.</bold><hr></hr></th><th><bold>Zhang et al.</bold><hr></hr></th><th><bold>Zhao et al.</bold><hr></hr></th><th><bold>Sun et al.</bold> [<xref rid="bb0100" ref-type="bibr">20</xref>]<hr></hr></th><th><bold>Li et al.</bold> [<xref rid="bb0105" ref-type="bibr">21</xref>]<hr></hr></th><th><bold>Su et al.</bold> [<xref rid="bb0110" ref-type="bibr">22</xref>]<hr></hr></th><th><bold>Qiu et al.</bold> [<xref rid="bb0115" ref-type="bibr">23</xref>]<hr></hr></th><th><bold>Lin et al.</bold> [<xref rid="bb0120" ref-type="bibr">24</xref>]<hr></hr></th><th><bold>Zheng et al.</bold> [<xref rid="bb0125" ref-type="bibr">25</xref>]<hr></hr></th><th><bold>Dong et al.</bold> [<xref rid="bb0015" ref-type="bibr">3</xref>]<hr></hr></th></tr><tr><th colspan="12"><bold>Summarised in Henry et al.</bold> [<xref rid="bb0010" ref-type="bibr">2</xref>]</th><th></th><th></th><th></th><th></th><th></th><th></th><th><bold>CDC data</bold></th></tr></thead><tbody><tr><td><bold>No of cases</bold></td><td>10</td><td>1</td><td>1</td><td>15</td><td>31</td><td>1</td><td>1</td><td>1</td><td>1</td><td>1</td><td>2</td><td>1</td><td>8</td><td>2</td><td>9</td><td>36</td><td>1</td><td>25</td><td>2143</td></tr><tr><td><bold>Age (median; range)</bold></td><td>6 yr (3mo-11 yr)</td><td>7 yr</td><td>13mo</td><td>12 yr</td><td>7 yr (6mo-17 yr)</td><td>2wk</td><td>3mo</td><td>7 yr</td><td>6mo</td><td>10 yr</td><td>14mo (twins)</td><td>13 yr</td><td>5 yr (2mo-15 yr)</td><td>4 yr (4 yr)</td><td>3.6 yr (11mo-9 yr)</td><td>8.3 (1-16 yr)</td><td>7 yr</td><td>3 yr (2-9 yr)</td><td>7 yr (2-13yyr)</td></tr><tr><td><bold>Region</bold></td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>Singapore</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td><td>China</td></tr><tr><td><bold>Males</bold></td><td>4 (40%)</td><td>1 (100%)</td><td>1 (100%)</td><td>5 (33%)</td><td>15 (48%)</td><td>1 (100%)</td><td>0</td><td>1 (100%)</td><td>1 (100%)</td><td>1 (100%)</td><td>0</td><td>1 (100%)</td><td>6 (75%)</td><td>1 (500%)</td><td>3 (33%)</td><td>23 (64%)</td><td>0</td><td>14 (56%)</td><td>1213 (56.6%)</td></tr><tr><td><bold>Symptoms</bold></td><td>10 (100%), mild</td><td>1 (100%), mild</td><td>1 (100%), mild</td><td>3 (20%), mild</td><td>27 (87%), mild</td><td>1 (100%), mild</td><td>1 (100%), mild</td><td>1 (100%), mild</td><td>0</td><td>0</td><td>2 (100%), mild</td><td>1 (100%), mild</td><td><bold><italic>8 (100%), severe or critical</italic></bold></td><td>2 (100%), moderate</td><td>3 (33%), mild to moderate</td><td>36 (100%), 17 (47.2%) mild, 19 (52.8%) moderate</td><td>1 (100%), mild</td><td>25 (100%), 8 (32)mild, 15 (60%) moderate, 2 (8%) severe</td><td>2047 (94.9%), 1091 (50.9%) mild, 831 (38.8%) moderate, <bold><italic>112 (5.2%) severe, 13 (0.6% critical)</italic></bold></td></tr><tr><td><bold>Chest radiographic changes</bold></td><td>4 (40%)</td><td>1 (100%)</td><td>1 (100%)</td><td>9 (60%)</td><td>14 (45%)</td><td>1 (100%)</td><td>1 (100%)</td><td>1 (100%)</td><td>0</td><td>1 (100%)</td><td>1 (50%)</td><td>1 (100%)</td><td>8 (100%)</td><td>2 (100%)</td><td>5 (55.5%)</td><td>19 (53%), all in moderate disease</td><td>0</td><td>17 (68%)</td><td>N/A</td></tr><tr><td><bold>WBC↑</bold></td><td>3 (30%)</td><td>1 (100%)</td><td>1 (100%)</td><td>0</td><td>3 (9.7%)</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>2 (100%)</td><td>0</td><td>2 (25%)</td><td>0</td><td>0</td><td>0</td><td>0</td><td>0</td><td>N/A</td></tr><tr><td><bold>WBC↓</bold></td><td>1 (10%)</td><td>0</td><td>0</td><td>7 (15%)</td><td>2 (6.5%)</td><td>0</td><td>0</td><td>0</td><td>1 (100%)</td><td>0</td><td>0</td><td>0</td><td>1 (12.5%)</td><td>0</td><td>3 (33%)</td><td>7 (19.4%)</td><td>0</td><td>0</td><td>N/A</td></tr><tr><td><bold>Lymphocytes ↑</bold></td><td>1 (10%)↑</td><td>N/A</td><td>1 (100%)</td><td>N/A</td><td>4 (12.9%)</td><td>N/A</td><td>N/A</td><td>0</td><td>0</td><td>0</td><td>N/A</td><td>0</td><td>0</td><td>0</td><td>0</td><td>11 (30.5%)↓</td><td>0</td><td>0</td><td>N/A</td></tr><tr><td><bold>Lymphocytes ↓</bold></td><td>0</td><td>N/A</td><td>0</td><td>N/A</td><td>2 (6.5%)</td><td>N/A</td><td>N/A</td><td>0</td><td>1 (100%)</td><td>0</td><td></td><td>0</td><td>1 (12.5%)</td><td>0</td><td>0</td><td></td><td>0</td><td>0</td><td>N/A</td></tr><tr><td><bold>HB↓</bold></td><td>0</td><td>N/A</td><td>1 (100%)</td><td>N/A</td><td>N/A</td><td>0</td><td>0</td><td>N/A</td><td>N/A</td><td>0</td><td>0</td><td>0</td><td>3 (37.5%)</td><td>N/A</td><td>5 (55%)</td><td>N/A</td><td>0</td><td>N/A</td><td>N/A</td></tr><tr><td><bold>PLT↑</bold></td><td>2 (20%)</td><td>0</td><td>0</td><td>N/A</td><td>2 (6.5%)</td><td>1 (100%)</td><td>1 (100%)</td><td>0</td><td>0</td><td>0</td><td>2 (100%)</td><td>0</td><td>2 (25%)</td><td>N/A</td><td>0</td><td>N/A</td><td>0</td><td>N/A</td><td>N/A</td></tr><tr><td><bold>PLT↓</bold></td><td>1(10%)</td><td>1 (100%)</td><td>0</td><td>N/A</td><td>0</td><td>0</td><td>0</td><td>0</td><td>1 (100%)</td><td>0</td><td>0</td><td>0</td><td>1 (12.5%)</td><td>N/A</td><td>1 (11%)</td><td></td><td>0</td><td></td><td></td></tr><tr><td><bold>CRP ↑</bold></td><td>3 (30%)</td><td>1 (100%)</td><td>1 (100%)</td><td>N/A</td><td>3 (9.7%), N/A for 1 (3.2%)</td><td>0</td><td>0</td><td>0</td><td>N/A</td><td>0</td><td>1 (50%)</td><td>0</td><td>5 (62.5%)</td><td>1 (50%)</td><td>0</td><td>1 (2.0%)</td><td>0</td><td>N/A, median 14.5 mg/L 0.91–25.04) (Normal: <10 ml/L)</td><td>N/A</td></tr><tr><td><bold>ESR ↑</bold></td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>N/A</td><td>0</td><td>N/A</td><td>N/A</td><td>0</td><td>0</td><td>N/A</td><td>N/A</td><td>N/A</td></tr><tr><td><bold>LFT↑</bold></td><td>2 (20%)</td><td>0</td><td>N/A</td><td>N/A</td><td>7 (22%)</td><td>N/A</td><td>N/A</td><td>0</td><td>N/A</td><td>0</td><td>2 (100%)</td><td>0</td><td>3 (37.5%)</td><td>0</td><td>0</td><td>3 (8.3%</td><td>0</td><td>0</td><td>N/A</td></tr></tbody></table><table-wrap-foot><fn><p>Currently available datasets are from Chinese cohorts. Most children experienced mild or moderate disease, while 133 of 2290 children summarised in <xref rid="t0005" ref-type="table">Table 1</xref> were severely or critically ill (<bold><italic>bold italics</italic></bold>) (5.8%), and 2 died (0.09%). Few children who developed severe COVID-19 did not consistently exhibit clinical and/or laboratory signs of cytokine storm syndromes, such as cytopenias, or altered liver function. While data are very limited, this appears to be in contrast to adult cohorts, where significant proportions of severely ill patients show signs of cytokine storm syndrome, which is associated with poor outcomes [<xref rid="bb0005" ref-type="bibr">1</xref>,<xref rid="bb0045" ref-type="bibr">9</xref>]. <bold>Abbreviations:</bold> WBC: white blood counts, HB: haemoglobin, PLT: Platelet counts, CRP: C reactive protein, ESR: erythrocyte sedimentation rate, LFT: liver function tests (AST and/or ALT elevation), N/A: not available.</p></fn></table-wrap-foot></table-wrap></p><p id="p0040">Molecular studies targeting the pathophysiology of COVID-19 are sparse, but clinical and molecular parallels with related coronaviruses (SARS-, MERS-CoV) may be extrapolated.</p></sec><sec id="s0010"><label>2</label><title>Infection and immune evasion</title><p id="p0045">Both SARS-CoV and SARS-Cov2 use ACE2 as entry receptor facilitating infection. Reflecting common organ involvement, ACE2 is expressed on pulmonary and intestinal epithelial cells [<xref rid="bb0005" ref-type="bibr">1</xref>,<xref rid="bb0020" ref-type="bibr">4</xref>]. As ACE2 is only expressed on a small subset of immune cells, other receptors and/or phagocytosis of virus-containing immune complexes may be involved in their infection [<xref rid="bb0005" ref-type="bibr">1</xref>,<xref rid="bb0025" ref-type="bibr">5</xref>,<xref rid="bb0030" ref-type="bibr">6</xref>].</p><p id="p0050">SARS-CoV and SARS-CoV2 share the potential to escape the host's immune response [<xref rid="bb0030" ref-type="bibr">6</xref>]. Usually, RNAs viruses, including coronaviruses, are detected by endosomal TLR-3 and 7 and/or cytoplasmic RNA sensors RIG-I and MDA5. TLR-3 and -7 promote nuclear shuttling of transcription factors NFκB and IRF3, while RIG-1/MDA5 ligation results in activation of IRF3. This triggers increased expression of type 1 interferons (T1IFN) (through IRF3) and other innate pro-inflammatory cytokines (IL-1, IL-6, TNF-α through NFκB) [<xref rid="bb0030" ref-type="bibr">6</xref>,<xref rid="bb0035" ref-type="bibr">7</xref>]. These induce an “anti-viral state” and innate and adaptive immune cell responses which contribute to pathogen containment and clearance. Novel coronaviruses can escape these mechanisms by altering ubiquitination and degradation of the RIG-I/MDA5 adaptor molecule mitochondrial antiviral-signalling protein (MAVS), and inhibition of the nuclear translocation of IRF3 and TNF receptor-associated factors (TRAF)3 and 6 which induce NFκB signalling [<xref rid="bb0040" ref-type="bibr">8</xref>]. Furthermore, SARS-CoV and SARS-CoV-2 can counteract T1IFN through inhibition of STAT transcription factor phosphorylation [<xref rid="bb0035" ref-type="bibr">7</xref>].</p></sec><sec id="s0015"><label>3</label><title>COVID-19 associated cytokine storm</title><p id="p0055">Several clinical and laboratory features of COVID-19 are associated with poor outcomes. Early studies from China linked cytopenias (leukopenia, lymphopenia, anaemia, thrombcytopenia) and elevated inflammatory parameters (IL-6, CRP, ESR) with unfavourable outcomes, suggesting cytokine storm syndrome in these patients [<xref rid="bb0045" ref-type="bibr">9</xref>]. ICU dependency in particular was associated with increased plasma levels of innate chemokines IP<italic>-</italic>10, MCP-1, MIP-1A, and the pro-inflammatory cytokine TNF-α [<xref rid="bb0050" ref-type="bibr">10</xref>].</p><p id="p0060">Though seemingly contradictory to aforementioned immune evasion through reduced cytokine expression, enhanced innate immune activation promotes morbidity and mortality in COVID-19. However, possible contributors to uncontrolled inflammation are cell damage and death as a result of viral replication [<xref rid="bb0055" ref-type="bibr">11</xref>]. In SARS-CoV infected mice, innate immune cells are recruited to the site of infection, where they induce strong inflammatory responses that further promote tissue damage and systemic inflammation [<xref rid="bb0060" ref-type="bibr">12</xref>].</p><p id="p0065">Another mechanism contributing to poor outcomes may be antibody-dependent enhancement which is caused by early antibody production. Resulting virus-containing immune complexes promote cellular uptake of virus particles through Fcγ receptors. This may result in persistent viral replication in cells (including antigen-presenting cells), and immune complex mediated inflammation and damage [<xref rid="bb0065" ref-type="bibr">[13]</xref>, <xref rid="bb0070" ref-type="bibr">[14]</xref>, <xref rid="bb0075" ref-type="bibr">[15]</xref>]. Indeed, blood vessel occlusion and infarctions have been reported in COVID, and show histopathologic features associated with immune complex vasculitis [<xref rid="bb0060" ref-type="bibr">12</xref>].</p></sec><sec id="s0020"><label>4</label><title>Why do children not get sicker?</title><p id="p0070">Currently, it is not known why children usually develop mild/moderate disease and only rarely develop cytokine storm syndrome (<xref rid="t0005" ref-type="table">Table 1</xref>). Several contributors may alter risk in children:<list list-type="simple" id="l0010"><list-item id="li0030"><label>i)</label><p id="p0075">Children are not travelling for business, reducing exposure to people. This may have played a role at the beginning of the pandemic.</p></list-item><list-item id="li0035"><label>ii)</label><p id="p0080">While pathogen clearance may be reduced in adults, particularly in individuals at risk (elderly patients, diabetics, etc.) [<xref rid="bb0030" ref-type="bibr">6</xref>,<xref rid="bb0050" ref-type="bibr">10</xref>], children have fewer comorbidities, including obesity.</p></list-item><list-item id="li0040"><label>iii)</label><p id="p0085">Different immune response compared to adults, including strong innate and weaker adaptive immune responses. This may contribute to effective virus containment/clearance and/or reduced secondary lymphocyte-mediated inflammation [<xref rid="bb0080" ref-type="bibr">16</xref>].</p></list-item><list-item id="li0045"><label>iv)</label><p id="p0090">Local microbiomes, co-infections (and co-clearance) with other viruses, and/or immune priming to coronavirus infections as a result of frequent/constant exposure may help children to overcome SARS-CoV2 more effectively.</p></list-item><list-item id="li0050"><label>v)</label><p id="p0095">As ACE2 is essential for epithelial cell infection, but also controls pulmonary inflammation and repair, variable ACE2 expression patterns may affect disease susceptibility and progression [<xref rid="bb0085" ref-type="bibr">17</xref>,<xref rid="bb0090" ref-type="bibr">18</xref>].</p></list-item></list></p></sec><sec id="s0025"><label>5</label><title>Risk for patients receiving immunosuppressive treatment</title><p id="p0100">Coronaviruses, including SARS-CoV2 are “masters” of immune evasion, which contributes to uncontrolled virus replication and delayed but significant pro-inflammatory cytokine responses. While most children and young people effectively control infections and less frequently develop severe disease, patients receiving immune modulating treatments may have reduced ability to do so. Reassuringly, in a cohort of 200 liver transplant patients on immune suppressive treatment, only three tested positive for SARS-CoV2 and none developed relevant disease [<xref rid="bb0095" ref-type="bibr">19</xref>].</p><p id="p0105">There are no evidence-based, approved treatments for COVID-19 and/or associated cytokine storm syndromes. Though children receiving immunosuppressive treatment may be at an increased risk for SARS-CoV2 infections, immunosuppression may protect from complications. Antimalarial treatments (chloroquine/hydroxychloroquine) may prevent infection through endocytosis. Classical and/or biologic DMARDs (particularly IL-6 and IL-1 blockers) may control pro-inflammatory cytokine expression and limit tissue/organ damage. Delayed activation of adaptive immune responses may be of benefit, as early antibody production may promote infection of immune cells and/or cause immune complex mediated pathology [<xref rid="bb0075" ref-type="bibr">15</xref>].</p></sec><sec id="s0030"><label>6</label><title>Conclusions</title><p id="p0110">While data on COVID-19 is limited, children appear to be protected from severe disease. Paediatric Rheumatology Societies, including the Paediatric Rheumatology European Society (<ext-link ext-link-type="uri" xlink:href="https://www.pres.eu/news/newsstory.html?id=29" id="ir0005">https://www.pres.eu/news/newsstory.html?id=29</ext-link>), recognize that discontinuation of immune modulating treatment may result in disease flares. In the absence of symptoms, immune modulating treatment should therefore be continued and changes should only be made under close monitoring by the responsible clinical service. 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