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المؤلفGheyath K., Nasrallah
تاريخ الإتاحة2022-09-04T07:38:01Z
تاريخ النشر2022-02-28
اسم المنشورeBioMedicine
المعرّفhttp://dx.doi.org/10.1016/j.ebiom.2022.103831
الرقم المعياري الدولي للكتاب23523964
معرّف المصادر الموحدhttps://www.sciencedirect.com/science/article/pii/S2352396422000159
معرّف المصادر الموحدhttp://hdl.handle.net/10576/33667
الملخصBecause of the emergence of coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2), many questions remain unresolved regarding the abundance of cross-reactivity between the SARS-CoV-2 and other human seasonal coronaviruses (sCoVs) antigens and the role of the sCoVs preexisting antibodies in protective immunity to SARS-CoV-2. Four endemic human sCoVs (NL63, 229E, OC43, and HKU1), which cause the common cold and recurrent respiratory disease, are highly prevalent worldwide. While almost everyone has been exposed to at least one of these sCoVs, immune response to each sCoV declines over time.1 These human sCoVs share striking sequence similarities with the E-envelope (96%), M-membrane (91%), and N-nucleocapsid (91%) proteins of SARS-CoV-2.2 However, they only share about 24–30% similarities with the trimeric spike S-protein (S-trimer). The S-protein is considered the major target protein/antigen for the protective humoral and cellular immunity. That is, the S-protein contains the angiotensin-converting enzyme 2 (ACE2) receptor binding domain (known as S-RBD) that is important for viral cell entry.2 Due to the apparent similarities between sCoVs, cross-reactivity between antibodies elicited by different sCoVs and cognate antibodies targeting SARS-CoV-2 antigens is expected.2
اللغةen
الناشرElsevier
الموضوعsCoV
Preexisting immunity
SARS-CoV-2
Cross-protectivity
العنوانDo preexisting antibodies against seasonal coronaviruses have a protective role against SARS-CoV-2 infections and impact on COVID-19 severity?
النوعArticle
رقم المجلد76
Open Access user License http://creativecommons.org/licenses/by/4.0/
dc.accessType Open Access


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