Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection in Children and Adolescents

Castagnoli, Riccardo; Votto, Martina; Brambilla, Ilaria; Bruno, Raffaele; Perlini, Stefano; Rovida, Francesca; Baldanti, Fausto

doi:10.1001/jamapediatrics.2020.1467

Cited by 1,063 publications

(1,111 citation statements)

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“…Nevertheless, prior immunity induced by one HCoV has also been reported to reduce the transmission of homologous and, importantly, heterologous HCoVs, and to ameliorate the symptoms where transmission is not prevented 1,4,5 . A possible modification of COVID-19 severity by prior HCoV infection might account for the age distribution of COVID-19 susceptibility, where higher HCoV infection rates in children than in adults 5,34,35 , correlates with relative protection from COVID-19 36 . Public health measures intended to prevent the spread of SARS-CoV-2 will also prevent the spread of and, consequently, maintenance of herd immunity to HCoVs, particularly in children.…”

Section: Discussionmentioning

confidence: 99%

Pre-existing and de novo humoral immunity to SARS-CoV-2 in humans

Ng¹,

Faulkner²,

Cornish³

et al. 2020

Preprint

126

170

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Several related human coronaviruses (HCoVs) are endemic in the human population, causing mild respiratory infections 1 . Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiologic agent of Coronavirus disease 2019 , is a recent zoonotic infection that has quickly reached pandemic spread 2,3 . Zoonotic introduction of novel coronaviruses is thought to occur in the absence of pre-existing immunity in the target human population. Using diverse assays for detection of antibodies reactive with the SARS-CoV-2 Spike (S) glycoprotein, we demonstrate the presence of pre-existing immunity in uninfected and unexposed humans to the new coronavirus. SARS-CoV-2 S-reactive antibodies, exclusively of the IgG class, were readily detectable by a sensitive flow cytometry-based method in SARS-CoV-2-uninfected individuals with recent HCoV infection and targeted the S2 subunit. In contrast, SARS-CoV-2 infection induced higher titres of SARS-CoV-2 Sreactive IgG antibodies, as well as concomitant IgM and IgA antibodies throughout the observation period of 6 weeks since symptoms onset. HCoV patient sera also variably reacted with SARS-CoV-2 S and nucleocapsid (N), but not with the S1 subunit or the receptor binding domain (RBD) of S on standard enzyme immunoassays. Notably, HCoV patient sera exhibited specific neutralising activity against SARS-CoV-2 S pseudotypes, according to levels of SARS-CoV-2 S-binding IgG and with efficiencies comparable to those of COVID-19 patient sera. Distinguishing pre-existing and de novo antibody responses to SARS-CoV-2 will be critical for serology, seroprevalence and vaccine studies, as well as for our understanding of susceptibility to and natural course of SARS-CoV-2 infection. ResultsImmune cross-reactivity among seasonally spreading human coronaviruses (HCoVs) has long been hypothesised to provide cross-protection, albeit transient, against infection with distinct HCoV types 1,4,5 . To determine the degree of cross-reactivity between HCoVs and the recently introduced zoonotic coronavirus SARS-CoV-2, we developed a sensitive flow cytometry-based assay for detection of SARS-CoV-2-binding antibodies. Sera from COVID-19 patients at University College London Hospitals (UCLH) (Table S1), contained high levels of IgG, IgM and IgA antibodies recognising the wild-type Spike (S) glycoprotein of SARS-CoV-2 expressed on the surface of HEK293T cells, whereas control sera did not (Fig. 1a). Notably, sera from a proportion patients with confirmed HCoV infection collected before or during the early spread of SARS-CoV-2 in the UK (Table S1), also contained SARS-CoV-2 S-specific antibodies (Fig. 1a). However, the latter sera contained only lower levels of S-specific IgG and no IgM or IgA antibodies, which clearly distinguished them from COVID-19 patient sera (Fig. 1a). The SARS-CoV-2 S protein is proteolytically processed into the S1 and S2 subunits that mediate target cell attachment and entry, respectively 6,7 . S2 exhibits a higher degree of homology among coronaviruses than S1 (Extended data Fig. 1...

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Section: Discussionmentioning

confidence: 99%

Pre-existing and de novo humoral immunity to SARS-CoV-2 in humans

Ng¹,

Faulkner²,

Cornish³

et al. 2020

Preprint

126

170

View full text Add to dashboard Cite

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“…After removing duplicates, the first search yielded eight systematic reviews [5,[7][8][9][10][11][12][13]. Three of them were eliminated because they did include information on clinical characteristics in children [7][8][9].…”

Section: Resultsmentioning

confidence: 99%

“…Three of them were eliminated because they did include information on clinical characteristics in children [7][8][9]. Therefore, we evaluated five systematic reviews done at different periods during the pandemic and thus including somewhat different primary studies [10][11][12][13] [13] included 45 studies from China (the total number of patients was not described) up to March 19, 2020. And Streng et al [14] included 8 studies from China (ranging from 6 to 2,143 patients) and one survey from Germany (33 patients) in hospitalized children, up to March 31, 2020.…”

Section: Resultsmentioning

confidence: 99%

Asthma and COVID-19 in children – a systematic review and call for data

Castro-Rodriguez

Forno

2020

Preprint

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Rationale:Whether asthma constitutes a risk factor for COVID-19 is unclear. Methods:We performed a systematic literature search in three stages: First, we reviewed PubMed, EMBASE and CINAHL for systematic reviews of SARS-CoC-2 and COVID-19 in pediatric populations, and reviewed their primary articles; next, we searched PubMed for studies on COVID-19 or SARS-CoV-2 and asthma/wheeze, and evaluated whether the resulting studies included pediatric populations; lastly, we repeated the second search in BioRxiv.org and MedRxiv.org to find pre-prints that may have information on pediatric asthma. Results:In the first search, eight systematic reviews were found, of which five were done in pediatric population; after reviewing 67 primary studies we found no data on pediatric asthma as a comorbidity for COVID-19. In the second search, we found 25 results in PubMed, of which five reported asthma in adults, but none included data on children. In the third search, 14 preprints in MedRxiv were identified with data on asthma, but again none with pediatric data. We found only one report by the U.S. CDC stating that 40/345 (~11.5%) children with data on chronic conditions had "chronic lung diseases including asthma". Conclusion:There is scarcely any data on whether childhood asthma (or other pediatric respiratory diseases) constitute risk factors for SARS-CoV-2 infection or COVID-19 severity. Studies are needed that go beyond counting the number of cases in the pediatric age range.

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“…This observation is quite in consistent with the ndings of large epidemiological studies. Children who get SARS-CoV-2 infection mostly have mild respiratory symptoms or are asymptomatic [24].Elderly patients with COVID-19, especially male patients, are more likely to progress into severe-type and even die of this disease [25,26]. Thus, difference in the immune response to the same SARS-CoV-2 virus between children and elderly male patients should be essential in elucidating the mechanisms by which severe COVID-19 is generated.…”

Section: Discussionmentioning

confidence: 99%

Presymptomatic Transmission and Diverse Progression of Familial Clustering Covid-19 Cases in Zhoushan, China

Liu

Liu²,

et al. 2020

Preprint

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Background Novel coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-caused emerging infectious disease, firstly identified in Wuhan (Hubei, China), is pandemic. However, data concerning presymptomatic SARS-CoV-2 transmission and disease diversity among family members are limited. Herein, We investigated the epidemiological and clinical characteristics of presymptomatic transmission-caused familial clustering cases of SARS-CoV-2 infection in Zhoushan island, China. Methods All family members were tested for SARS-CoV-2 genomic RNA by quantitative reverse transcription PCR in 3 different samples and serum antibody immunoglobin M (IgM) and IgG against SARS-CoV-2. Exposure identification, laboratory test, and imaging were performed according to the national guideline of COVID-19 (7th edition, China). Results Of the 6 cases, index case who ever met his relative with COVID-19 from Xianning, Hubei on January 26–31, 2020, transmitted SARS-CoV-2 to his family members in Zhoushan via visiting family during January 31 and February 3, 2020. The index was identified as common-type COVID-19 on February 6, 2020. All 5 family members were infected with SARS-CoV-2. Of those, a 7-year-old girl was an asymptomatic carrier whereas her grandparents, especially her grandfather, were very sick. Case 6 (grandfather) remained positive for SARS-CoV-2 RNA in his sputum specimen in subsequent 2 months. Case 2 (mother) tested negative for SARS-CoV-2 RNA in all samples but positive for IgM and IgG to SARS-CoV-2 since February 9, 2020. Conclusions Presymptomatic transmission of SARS-CoV-2 causes familial cluster of COVID-19. Exposed to the same source of infection, family members present their differences in disease severity and viral clearance.

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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection in Children and Adolescents

Cited by 1,063 publications

References 34 publications

Pre-existing and de novo humoral immunity to SARS-CoV-2 in humans

Pre-existing and de novo humoral immunity to SARS-CoV-2 in humans

Asthma and COVID-19 in children – a systematic review and call for data

Presymptomatic Transmission and Diverse Progression of Familial Clustering Covid-19 Cases in Zhoushan, China

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