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Tran, Khanh Bao, Lang, Justin J.; Compton, Kelly, Xu, Rixing, Acheson, Alistair R.; Henrikson, Hannah Jacqueline, Kocarnik, Jonathan M.; Penberthy, Louise, Aali, Amirali, Abbas, Qamar, Abbasi, Behzad, Abbasi-Kangevari, Mohsen, Abbasi-Kangevari, Zeinab, Abbastabar, Hedayat, Abdelmasseh, Michael, Abd-Elsalam, Sherief, Abdelwahab, Ahmed Abdelwahab, Abdoli, Gholamreza, Abdulkadir, Hanan Abdulkadir, Abedi, Aidin, Abegaz, Kedir Hussein, Abidi, Hassan, Aboagye, Richard Gyan, Abolhassani, Hassan, Absalan, Abdorrahim, Abtew, Yonas Derso, Abubaker Ali, Hiwa, Abu-Gharbieh, Eman, Achappa, Basavaprabhu, Acuna, Juan Manuel, Addison, Daniel, Addo, Isaac Yeboah, Adegboye, Oyelola A.; Adesina, Miracle Ayomikun, Adnan, Mohammad, Adnani, Qorinah Estiningtyas Sakilah, Advani, Shailesh M.; Afrin, Sumia, Afzal, Muhammad Sohail, Aggarwal, Manik, Ahinkorah, Bright Opoku, Ahmad, Araz Ramazan, Ahmad, Rizwan, Ahmad, Sajjad, Ahmad, Sohail, Ahmadi, Sepideh, Ahmed, Haroon, Ahmed, Luai A.; Ahmed, Muktar Beshir, Ahmed Rashid, Tarik, Aiman, Wajeeha, Ajami, Marjan, Akalu, Gizachew Taddesse, Akbarzadeh-Khiavi, Mostafa, Aklilu, Addis, Akonde, Maxwell, Akunna, Chisom Joyqueenet, Al Hamad, Hanadi, Alahdab, Fares, Alanezi, Fahad Mashhour, Alanzi, Turki M.; Alessy, Saleh Ali, Algammal, Abdelazeem M.; Al-Hanawi, Mohammed Khaled, Alhassan, Robert Kaba, Ali, Beriwan Abdulqadir, Ali, Liaqat, Ali, Syed Shujait, Alimohamadi, Yousef, Alipour, Vahid, Aljunid, Syed Mohamed, Alkhayyat, Motasem, Al-Maweri, Sadeq Ali Ali, Almustanyir, Sami, Alonso, Nivaldo, Alqalyoobi, Shehabaldin, Al-Raddadi, Rajaa M.; Al-Rifai, Rami H. Hani, Al-Sabah, Salman Khalifah, Al-Tammemi, Ala'a B.; Altawalah, Haya, Alvis-Guzman, Nelson, Amare, Firehiwot, Ameyaw, Edward Kwabena, Aminian Dehkordi, Javad Javad, Amirzade-Iranaq, Mohammad Hosein, Amu, Hubert, Amusa, Ganiyu Adeniyi, Ancuceanu, Robert, Anderson, Jason A.; Animut, Yaregal Animut, Anoushiravani, Amir, Anoushirvani, Ali Arash, Ansari-Moghaddam, Alireza, Ansha, Mustafa Geleto, Antony, Benny, Antwi, Maxwell Hubert, Anwar, Sumadi Lukman, Anwer, Razique, Anyasodor, Anayochukwu Edward, Arabloo, Jalal, Arab-Zozani, Morteza, Aremu, Olatunde, Argaw, Ayele Mamo, Ariffin, Hany, Aripov, Timur, Arshad, Muhammad, Artaman, Al, Arulappan, Judie, Aruleba, Raphael Taiwo, Aryannejad, Armin, Asaad, Malke, Asemahagn, Mulusew A.; Asemi, Zatollah, Asghari-Jafarabadi, Mohammad, Ashraf, Tahira, Assadi, Reza, Athar, Mohammad, Athari, Seyyed Shamsadin, Atout, Maha Moh'd Wahbi, Attia, Sameh, Aujayeb, Avinash, Ausloos, Marcel, Avila-Burgos, Leticia, Awedew, Atalel Fentahun, Awoke, Mamaru Ayenew, Awoke, Tewachew, Ayala Quintanilla, Beatriz Paulina, Ayana, Tegegn Mulatu, Ayen, Solomon Shitu, Azadi, Davood, Azadnajafabad, Sina, Azami-Aghdash, Saber, Azanaw, Melkalem Mamuye, Azangou-Khyavy, Mohammadreza, Azari Jafari, Amirhossein, Azizi, Hosein, Azzam, Ahmed Y. Y.; Babajani, Amirhesam, Badar, Muhammad, Badiye, Ashish D.; Baghcheghi, Nayereh, Bagheri, Nader, Bagherieh, Sara, Bahadory, Saeed, Baig, Atif Amin, Baker, Jennifer L.; Bakhtiari, Ahad, Bakshi, Ravleen Kaur, Banach, Maciej, Banerjee, Indrajit, Bardhan, Mainak, Barone-Adesi, Francesco, Barra, Fabio, Barrow, Amadou, Bashir, Nasir Z.; Bashiri, Azadeh, Basu, Saurav, Batiha, Abdul-Monim Mohammad, Begum, Aeysha, Bekele, Alehegn Bekele, Belay, Alemayehu Sayih, Belete, Melaku Ashagrie, Belgaumi, Uzma Iqbal, Bell, Arielle Wilder, Belo, Luis, Benzian, Habib, Berhie, Alemshet Yirga, Bermudez, Amiel Nazer C.; Bernabe, Eduardo, Bhagavathula, Akshaya Srikanth, Bhala, Neeraj, Bhandari, Bharti Bhandari, Bhardwaj, Nikha, Bhardwaj, Pankaj, Bhattacharyya, Krittika, Bhojaraja, Vijayalakshmi S.; Bhuyan, Soumitra S.; Bibi, Sadia, Bilchut, Awraris Hailu, Bintoro, Bagas Suryo, Biondi, Antonio, Birega, Mesfin Geremaw Birega, Birhan, Habitu Eshetu, Bjørge, Tone, Blyuss, Oleg, Bodicha, Belay Boda Abule, Bolla, Srinivasa Rao, Boloor, Archith, Bosetti, Cristina, Braithwaite, Dejana, Brauer, Michael, Brenner, Hermann, Briko, Andrey Nikolaevich, Briko, Nikolay Ivanovich, Buchanan, Christina Maree, Bulamu, Norma B.; Bustamante-Teixeira, Maria Teresa, Butt, Muhammad Hammad, Butt, Nadeem Shafique, Butt, Zahid A.; Caetano dos Santos, Florentino Luciano, Cámera, Luis Alberto, Cao, Chao, Cao, Yin, Carreras, Giulia, Carvalho, Márcia, Cembranel, Francieli, Cerin, Ester, Chakraborty, Promit Ananyo, Charalampous, Periklis, Chattu, Vijay Kumar, Chimed-Ochir, Odgerel, Chirinos-Caceres, Jesus Lorenzo, Cho, Daniel Youngwhan, Cho, William C. S.; Christopher, Devasahayam J.; Chu, Dinh-Toi, Chukwu, Isaac Sunday, Cohen, Aaron J.; Conde, Joao, Cortés, Sandra, Costa, Vera Marisa, Cruz-Martins, Natália, Culbreth, Garland T.; Dadras, Omid, Dagnaw, Fentaw Teshome, Dahlawi, Saad M. A.; Dai, Xiaochen, Dandona, Lalit, Dandona, Rakhi, Daneshpajouhnejad, Parnaz, Danielewicz, Anna, Dao, An Thi Minh, Darvishi Cheshmeh Soltani, Reza, Darwesh, Aso Mohammad, Das, Saswati, Davitoiu, Dragos Virgil, Davtalab Esmaeili, Elham, De la Hoz, Fernando Pio, Debela, Sisay Abebe, Dehghan, Azizallah, Demisse, Biniyam, Demisse, Fitsum Wolde, Denova-Gutiérrez, Edgar, Derakhshani, Afshin, Derbew Molla, Meseret, Dereje, Diriba, Deribe, Kalkidan Solomon, Desai, Rupak, Desalegn, Markos Desalegn, Dessalegn, Fikadu Nugusu, Dessalegni, Samuel Abebe A.; Dessie, Gashaw, Desta, Abebaw Alemayehu, Dewan, Syed Masudur Rahman, Dharmaratne, Samath Dhamminda, Dhimal, Meghnath, Dianatinasab, Mostafa, Diao, Nancy, Diaz, Daniel, Digesa, Lankamo Ena, Dixit, Shilpi Gupta, Doaei, Saeid, Doan, Linh Phuong, Doku, Paul Narh, Dongarwar, Deepa, dos Santos, Wendel Mombaque, Driscoll, Tim Robert, Dsouza, Haneil Larson, Durojaiye, Oyewole Christopher, Edalati, Sareh, Eghbalian, Fatemeh, Ehsani-Chimeh, Elham, Eini, Ebrahim, Ekholuenetale, Michael, Ekundayo, Temitope Cyrus, Ekwueme, Donatus U.; El Tantawi, Maha, Elbahnasawy, Mostafa Ahmed, Elbarazi, Iffat, Elghazaly, Hesham, Elhadi, Muhammed, El-Huneidi, Waseem, Emamian, Mohammad Hassan, Engelbert Bain, Luchuo, Enyew, Daniel Berhanie, Erkhembayar, Ryenchindorj, Eshetu, Tegegne, Eshrati, Babak, Eskandarieh, Sharareh, Espinosa-Montero, Juan, Etaee, Farshid, Etemadimanesh, Azin, Eyayu, Tahir, Ezeonwumelu, Ifeanyi Jude, Ezzikouri, Sayeh, Fagbamigbe, Adeniyi Francis, Fahimi, Saman, Fakhradiyev, Ildar Ravisovich, Faraon, Emerito Jose A.; Fares, Jawad, Farmany, Abbas, Farooque, Umar, Farrokhpour, Hossein, Fasanmi, Abidemi Omolara, Fatehizadeh, Ali, Fatima, Wafa, Fattahi, Hamed, Fekadu, Ginenus, Feleke, Berhanu Elfu, Ferrari, Allegra Allegra, Ferrero, Simone, Ferro Desideri, Lorenzo, Filip, Irina, Fischer, Florian, Foroumadi, Roham, Foroutan, Masoud, Fukumoto, Takeshi, Gaal, Peter Andras, Gad, Mohamed M.; Gadanya, Muktar A.; Gaipov, Abduzhappar, Galehdar, Nasrin, Gallus, Silvano, Garg, Tushar, Gaspar Fonseca, Mariana, Gebremariam, Yosef Haile, Gebremeskel, Teferi Gebru, Gebremichael, Mathewos Alemu, Geda, Yohannes Fikadu, Gela, Yibeltal Yismaw, Gemeda, Belete Negese Belete, Getachew, Melaku, Getachew, Motuma Erena, Ghaffari, Kazem, Ghafourifard, Mansour, Ghamari, Seyyed-Hadi, Ghasemi Nour, Mohammad, Ghassemi, Fariba, Ghimire, Ajnish, Ghith, Nermin, Gholamalizadeh, Maryam, Gholizadeh Navashenaq, Jamshid, Ghozy, Sherief, Gilani, Syed Amir, Gill, Paramjit Singh, Ginindza, Themba G.; Gizaw, Abraham Tamirat T.; Glasbey, James C.; Godos, Justyna, Goel, Amit, Golechha, Mahaveer, Goleij, Pouya, Golinelli, Davide, Golitaleb, Mohamad, Gorini, Giuseppe, Goulart, Bárbara Niegia Garcia, Grosso, Giuseppe, Guadie, Habtamu Alganeh, Gubari, Mohammed Ibrahim Mohialdeen, Gudayu, Temesgen Worku, Guerra, Maximiliano Ribeiro, Gunawardane, Damitha Asanga, Gupta, Bhawna, Gupta, Sapna, Gupta, Veer Bala, Gupta, Vivek Kumar, Gurara, Mekdes Kondale, Guta, Alemu, Habibzadeh, Parham, Haddadi Avval, Atlas, Hafezi-Nejad, Nima, Hajj Ali, Adel, Haj-Mirzaian, Arvin, Halboub, Esam S.; Halimi, Aram, Halwani, Rabih, Hamadeh, Randah R.; Hameed, Sajid, Hamidi, Samer, Hanif, Asif, Hariri, Sanam, Harlianto, Netanja I.; Haro, Josep Maria, Hartono, Risky Kusuma, Hasaballah, Ahmed I.; Hasan, S. M. Mahmudul, Hasani, Hamidreza, Hashemi, Seyedeh Melika, Hassan, Abbas M.; Hassanipour, Soheil, Hayat, Khezar, Heidari, Golnaz, Heidari, Mohammad, Heidarymeybodi, Zahra, Herrera-Serna, Brenda Yuliana, Herteliu, Claudiu, Hezam, Kamal, Hiraike, Yuta, Hlongwa, Mbuzeleni Mbuzeleni, Holla, Ramesh, Holm, Marianne, Horita, Nobuyuki, Hoseini, Mohammad, Hossain, Md Mahbub, Hossain, Mohammad Bellal Hossain, Hosseini, Mohammad-Salar, Hosseinzadeh, Ali, Hosseinzadeh, Mehdi, Hostiuc, Mihaela, Hostiuc, Sorin, Househ, Mowafa, Huang, Junjie, Hugo, Fernando N.; Humayun, Ayesha, Hussain, Salman, Hussein, Nawfal R.; Hwang, Bing-Fang, Ibitoye, Segun Emmanuel, Iftikhar, Pulwasha Maria, Ikuta, Kevin S.; Ilesanmi, Olayinka Stephen, Ilic, Irena M.; Ilic, Milena D.; Immurana, Mustapha, Innos, Kaire, Iranpour, Pooya, Irham, Lalu Muhammad, Islam, Md Shariful, Islam, Rakibul M.; Islami, Farhad, Ismail, Nahlah Elkudssiah, Isola, Gaetano, Iwagami, Masao, J, Linda Merin, Jaiswal, Abhishek, Jakovljevic, Mihajlo, Jalili, Mahsa, Jalilian, Shahram, Jamshidi, Elham, Jang, Sung-In, Jani, Chinmay T.; Javaheri, Tahereh, Jayarajah, Umesh Umesh, Jayaram, Shubha, Jazayeri, Seyed Behzad, Jebai, Rime, Jemal, Bedru, Jeong, Wonjeong, Jha, Ravi Prakash, Jindal, Har Ashish, John-Akinola, Yetunde O.; Jonas, Jost B.; Joo, Tamas, Joseph, Nitin, Joukar, Farahnaz, Jozwiak, Jacek Jerzy, Jürisson, Mikk, Kabir, Ali, Kacimi, Salah Eddine Oussama, Kadashetti, Vidya, Kahe, Farima, Kakodkar, Pradnya Vishal, Kalankesh, Laleh R.; Kalankesh, Leila R.; Kalhor, Rohollah, Kamal, Vineet Kumar, Kamangar, Farin, Kamath, Ashwin, Kanchan, Tanuj, Kandaswamy, Eswar, Kandel, Himal, Kang, HyeJung, Kanno, Girum Gebremeskel, Kapoor, Neeti, Kar, Sitanshu Sekhar, Karanth, Shama D.; Karaye, Ibraheem M.; Karch, André, Karimi, Amirali, Kassa, Bekalu Getnet, Katoto, Patrick D. M. C.; Kauppila, Joonas H.; Kaur, Harkiran, Kebede, Abinet Gebremickael, Keikavoosi-Arani, Leila, Kejela, Gemechu Gemechu, Kemp Bohan, Phillip M.; Keramati, Maryam, Keykhaei, Mohammad, Khajuria, Himanshu, Khan, Abbas, Khan, Abdul Aziz Khan, Khan, Ejaz Ahmad, Khan, Gulfaraz, Khan, Md Nuruzzaman, Khan, Moien A. B.; Khanali, Javad, Khatab, Khaled, Khatatbeh, Moawiah Mohammad, Khatib, Mahalaqua Nazli, Khayamzadeh, Maryam, Khayat Kashani, Hamid Reza, Khazeei Tabari, Mohammad Amin, Khezeli, Mehdi, Khodadost, Mahmoud, Kim, Min Seo, Kim, Yun Jin, Kisa, Adnan, Kisa, Sezer, Klugar, Miloslav, Klugarová, Jitka, Kolahi, Ali-Asghar, Kolkhir, Pavel, Kompani, Farzad, Koul, Parvaiz A.; Koulmane Laxminarayana, Sindhura Lakshmi, Koyanagi, Ai, Krishan, Kewal, Krishnamoorthy, Yuvaraj, Kucuk Bicer, Burcu, Kugbey, Nuworza, Kulimbet, Mukhtar, Kumar, Akshay, Kumar, G. Anil, Kumar, Narinder, Kurmi, Om P.; Kuttikkattu, Ambily, La Vecchia, Carlo, Lahiri, Arista, Lal, Dharmesh Kumar, Lám, Judit, Lan, Qing, Landires, Iván, Larijani, Bagher, Lasrado, Savita, Lau, Jerrald, Lauriola, Paolo, Ledda, Caterina, Lee, Sang-woong, Lee, Shaun Wen Huey, Lee, Wei-Chen, Lee, Yeong Yeh, Lee, Yo Han, Legesse, Samson Mideksa, Leigh, James, Leong, Elvynna, Li, Ming-Chieh, Lim, Stephen S.; Liu, Gang, Liu, Jue, Lo, Chun-Han, Lohiya, Ayush, Lopukhov, Platon D.; Lorenzovici, László, Lotfi, Mojgan, Loureiro, Joana A.; Lunevicius, Raimundas, Madadizadeh, Farzan, Mafi, Ahmad R.; Magdeldin, Sameh, Mahjoub, Soleiman, Mahmoodpoor, Ata, Mahmoudi, Morteza, Mahmoudimanesh, Marzieh, Mahumud, Rashidul Alam, Majeed, Azeem, Majidpoor, Jamal, Makki, Alaa, Makris, Konstantinos Christos, Malakan Rad, Elaheh, Malekpour, Mohammad-Reza, Malekzadeh, Reza, Malik, Ahmad Azam, Mallhi, Tauqeer Hussain, Mallya, Sneha Deepak, Mamun, Mohammed A.; Manda, Ana Laura, Mansour-Ghanaei, Fariborz, Mansouri, Borhan, Mansournia, Mohammad Ali, Mantovani, Lorenzo Giovanni, Martini, Santi, Martorell, Miquel, Masoudi, Sahar, Masoumi, Seyedeh Zahra, Matei, Clara N.; Mathews, Elezebeth, Mathur, Manu Raj, Mathur, Vasundhara, McKee, Martin, Meena, Jitendra Kumar, Mehmood, Khalid, Mehrabi Nasab, Entezar, Mehrotra, Ravi, Melese, Addisu, Mendoza, Walter, Menezes, Ritesh G.; Mengesha, SIsay Derso, Mensah, Laverne G.; Mentis, Alexios-Fotios A.; Mera-Mamián, Andry Yasmid Mera, Meretoja, Tuomo J.; Merid, Mehari Woldemariam, Mersha, Amanual Getnet, Meselu, Belsity Temesgen, Meshkat, Mahboobeh, Mestrovic, Tomislav, Miao Jonasson, Junmei, Miazgowski, Tomasz, Michalek, Irmina Maria, Mijena, Gelana Fekadu Worku, Miller, Ted R.; Mir, Shabir Ahmad, Mirinezhad, Seyed Kazem, Mirmoeeni, Seyyedmohammadsadeq, Mirza-Aghazadeh-Attari, Mohammad, Mirzaei, Hamed, Mirzaei, Hamid Reza, Misganaw, Abay Sisay, Misra, Sanjeev, Mohammad, Karzan Abdulmuhsin, Mohammadi, Esmaeil, Mohammadi, Mokhtar, Mohammadian-Hafshejani, Abdollah, Mohammadpourhodki, Reza, Mohammed, Arif, Mohammed, Shafiu, Mohan, Syam, Mohseni, Mohammad, Moka, Nagabhishek, Mokdad, Ali H.; Molassiotis, Alex, Molokhia, Mariam, Momenzadeh, Kaveh, Momtazmanesh, Sara, Monasta, Lorenzo, Mons, Ute, Montasir, Ahmed Al, Montazeri, Fateme, Montero, Arnulfo, Moosavi, Mohammad Amin, Moradi, Abdolvahab, Moradi, Yousef, Moradi Sarabi, Mostafa, Moraga, Paula, Morawska, Lidia, Morrison, Shane Douglas, Morze, Jakub, Mosapour, Abbas, Mostafavi, Ebrahim, Mousavi, Seyyed Meysam, Mousavi Isfahani, Haleh, Mousavi Khaneghah, Amin, Mpundu-Kaambwa, Christine, Mubarik, Sumaira, Mulita, Francesk, Munblit, Daniel, Munro, Sandra B.; Murillo-Zamora, Efrén, Musa, Jonah, Nabhan, Ashraf F.; Nagarajan, Ahamarshan Jayaraman, Nagaraju, Shankar Prasad, Nagel, Gabriele, Naghipour, Mohammadreza, Naimzada, Mukhammad David, Nair, Tapas Sadasivan, Naqvi, Atta Abbas, Narasimha Swamy, Sreenivas, Narayana, Aparna Ichalangod, Nassereldine, Hasan, Natto, Zuhair S.; Nayak, Biswa Prakash, Ndejjo, Rawlance, Nduaguba, Sabina Onyinye, Negash, Wogene Wogene, Nejadghaderi, Seyed Aria, Nejati, Kazem, Neupane Kandel, Sandhya, Nguyen, Huy Van Nguyen, Niazi, Robina Khan, Noor, Nurulamin M.; Noori, Maryam, Noroozi, Nafise, Nouraei, Hasti, Nowroozi, Ali, Nuñez-Samudio, Virginia, Nzoputam, Chimezie Igwegbe, Nzoputam, Ogochukwu Janet, Oancea, Bogdan, Odukoya, Oluwakemi Ololade, Oghenetega, Onome Bright, Ogunsakin, Ropo Ebenezer, Oguntade, Ayodipupo Sikiru, Oh, In-Hwan, Okati-Aliabad, Hassan, Okekunle, Akinkunmi Paul, Olagunju, Andrew T.; Olagunju, Tinuke O.; Olakunde, Babayemi Oluwaseun, Olufadewa, Isaac Iyinoluwa, Omer, Emad, Omonisi, Abidemi E. Emmanuel, Ong, Sokking, Onwujekwe, Obinna E.; Orru, Hans, Otstavnov, Stanislav S.; Oulhaj, Abderrahim, Oumer, Bilcha, Owopetu, Oluwatomi Funbi, Oyinloye, Babatunji Emmanuel, P A, Mahesh, Padron-Monedero, Alicia, Padubidri, Jagadish Rao, Pakbin, Babak, Pakshir, Keyvan, Pakzad, Reza, Palicz, Tamás, Pana, Adrian, Pandey, Anamika, Pandey, Ashok, Pant, Suman, Pardhan, Shahina, Park, Eun-Cheol, Park, Eun-Kee, Park, Seoyeon, Patel, Jay, Pati, Siddhartha, Paudel, Rajan, Paudel, Uttam, Paun, Mihaela, Pazoki Toroudi, Hamidreza, Peng, Minjin, Pereira, Jeevan, Pereira, Renato B.; Perna, Simone, Perumalsamy, Navaraj, Pestell, Richard G.; Pezzani, Raffaele, Piccinelli, Cristiano, Pillay, Julian David, Piracha, Zahra Zahid, Pischon, Tobias, Postma, Maarten J.; Pourabhari Langroudi, Ashkan, Pourshams, Akram, Pourtaheri, Naeimeh, Prashant, Akila, Qadir, Mirza Muhammad Fahd, Quazi Syed, Zahiruddin, Rabiee, Mohammad, Rabiee, Navid, Radfar, Amir, Radhakrishnan, Raghu Anekal, Radhakrishnan, Venkatraman, Raeisi, Mojtaba, Rafiee, Ata, Rafiei, Alireza, Raheem, Nasiru, Rahim, Fakher, Rahman, Md Obaidur, Rahman, Mosiur, Rahman, Muhammad Aziz, Rahmani, Amir Masoud, Rahmani, Shayan, Rahmanian, Vahid, Rajai, Nazanin, Rajesh, Aashish, Ram, Pradhum, Ramezanzadeh, Kiana, Rana, Juwel, Ranabhat, Kamal, Ranasinghe, Priyanga, Rao, Chythra R.; Rao, Sowmya J.; Rashedi, Sina, Rashidi, Amirfarzan, Rashidi, Mahsa, Rashidi, Mohammad-Mahdi, Ratan, Zubair Ahmed, Rawaf, David Laith, Rawaf, Salman, Rawal, Lal, Rawassizadeh, Reza, Razeghinia, Mohammad Sadegh, Rehman, Ashfaq Ur, Rehman, Inayat ur, Reitsma, Marissa B.; Renzaho, Andre M. N.; Rezaei, Maryam, Rezaei, Nazila, Rezaei, Negar, Rezaei, Nima, Rezaei, Saeid, Rezaeian, Mohsen, Rezapour, Aziz, Riad, Abanoub, Rikhtegar, Reza, Rios-Blancas, Maria, Roberts, Thomas J.; Rohloff, Peter, Romero-Rodríguez, Esperanza, Roshandel, Gholamreza, Rwegerera, Godfrey M.; S, Manjula, Saber-Ayad, Maha Mohamed, Saberzadeh-Ardestani, Bahar, Sabour, Siamak, Saddik, Basema, Sadeghi, Erfan, Saeb, Mohammad Reza, Saeed, Umar, Safaei, Mohsen, Safary, Azam, Sahebazzamani, Maryam, Sahebkar, Amirhossein, Sahoo, Harihar, Sajid, Mirza Rizwan, Salari, Hedayat, Salehi, Sana, Salem, Marwa Rashad, Salimzadeh, Hamideh, Samodra, Yoseph Leonardo, Samy, Abdallah M.; Sanabria, Juan, Sankararaman, Senthilkumar, Sanmarchi, Francesco, Santric-Milicevic, Milena M.; Saqib, Muhammad Arif Nadeem, Sarveazad, Arash, Sarvi, Fatemeh, Sathian, Brijesh, Satpathy, Maheswar, Sayegh, Nicolas, Schneider, Ione Jayce Ceola, Schwarzinger, Michaël, Šekerija, Mario, Senthilkumaran, Subramanian, Sepanlou, Sadaf G.; Seylani, Allen, Seyoum, Kenbon, Sha, Feng, Shafaat, Omid, Shah, Pritik A.; Shahabi, Saeed, Shahid, Izza, Shahrbaf, Mohammad Amin, Shahsavari, Hamid R.; Shaikh, Masood Ali, Shaka, Mohammed Feyisso, Shaker, Elaheh, Shannawaz, Mohammed, Sharew, Mequannent Melaku Sharew, Sharifi, Azam, Sharifi-Rad, Javad, Sharma, Purva, Shashamo, Bereket Beyene, Sheikh, Aziz, Sheikh, Mahdi, Sheikhbahaei, Sara, Sheikhi, Rahim Ali, Sheikhy, Ali, Shepherd, Peter Robin, Shetty, Adithi, Shetty, Jeevan K.; Shetty, Ranjitha S.; Shibuya, Kenji, Shirkoohi, Reza, Shirzad-Aski, Hesamaddin, Shivakumar, K. M.; Shivalli, Siddharudha, Shivarov, Velizar, Shobeiri, Parnian, Shokri Varniab, Zahra, Shorofi, Seyed Afshin, Shrestha, Sunil, Sibhat, Migbar Mekonnen, Siddappa Malleshappa, Sudeep K.; Sidemo, Negussie Boti, Silva, Diego Augusto Santos, Silva, Luís Manuel Lopes Rodrigues, Silva Julian, Guilherme, Silvestris, Nicola, Simegn, Wudneh, Singh, Achintya Dinesh, Singh, Ambrish, Singh, Garima, Singh, Harpreet, Singh, Jasvinder A.; Singh, Jitendra Kumar, Singh, Paramdeep, Singh, Surjit, Sinha, Dhirendra Narain, Sinke, Abiy H.; Siraj, Md Shahjahan, Sitas, Freddy, Siwal, Samarjeet Singh, Skryabin, Valentin Yurievich, Skryabina, Anna Aleksandrovna, Socea, Bogdan, Soeberg, Matthew J.; Sofi-Mahmudi, Ahmad, Solomon, Yonatan, Soltani-Zangbar, Mohammad Sadegh, Song, Suhang, Song, Yimeng, Sorensen, Reed J. D.; Soshnikov, Sergey, Sotoudeh, Houman, Sowe, Alieu, Sufiyan, Mu'awiyyah Babale, Suk, Ryan, Suleman, Muhammad, Suliankatchi Abdulkader, Rizwan, Sultana, Saima, Sur, Daniel, Szócska, Miklós, Tabaeian, Seidamir Pasha, Tabarés-Seisdedos, Rafael, Tabatabaei, Seyyed Mohammad, Tabuchi, Takahiro, Tadbiri, Hooman, Taheri, Ensiyeh, Taheri, Majid, Taheri Soodejani, Moslem, Takahashi, Ken, Talaat, Iman M.; Tampa, Mircea, Tan, Ker-Kan, Tat, Nathan Y.; Tat, Vivian Y.; Tavakoli, Ahmad, Tavakoli, Arash, Tehrani-Banihashemi, Arash, Tekalegn, Yohannes, Tesfay, Fisaha Haile, Thapar, Rekha, Thavamani, Aravind, Thoguluva Chandrasekar, Viveksandeep, Thomas, Nihal, Thomas, Nikhil Kenny, Ticoalu, Jansje Henny Vera, Tiyuri, Amir, Tollosa, Daniel Nigusse, Topor-Madry, Roman, Touvier, Mathilde, Tovani-Palone, Marcos Roberto, Traini, Eugenio, Tran, Mai Thi Ngoc, Tripathy, Jaya Prasad, Ukke, Gebresilasea Gendisha, Ullah, Irfan, Ullah, Saif, Ullah, Sana, Unnikrishnan, Bhaskaran, Vacante, Marco, Vaezi, Maryam, Valadan Tahbaz, Sahel, Valdez, Pascual R.; Vardavas, Constantine, Varthya, Shoban Babu, Vaziri, Siavash, Velazquez, Diana Zuleika, Veroux, Massimiliano, Villeneuve, Paul J.; Violante, Francesco S.; Vladimirov, Sergey Konstantinovitch, Vlassov, Vasily, Vo, Bay, Vu, Linh Gia, Wadood, Abdul Wadood, Waheed, Yasir, Walde, Mandaras Tariku, Wamai, Richard G.; Wang, Cong, Wang, Fang, Wang, Ning, Wang, Yu, Ward, Paul, Waris, Abdul, Westerman, Ronny, Wickramasinghe, Nuwan Darshana, Woldemariam, Melat, Woldu, Berhanu, Xiao, Hong, Xu, Suowen, Xu, Xiaoyue, Yadav, Lalit, Yahyazadeh Jabbari, Seyed Hossein, Yang, Lin, Yazdanpanah, Fereshteh, Yeshaw, Yigizie, Yismaw, Yazachew, Yonemoto, Naohiro, Younis, Mustafa Z.; Yousefi, Zabihollah, Yousefian, Fatemeh, Yu, Chuanhua, Yu, Yong, Yunusa, Ismaeel, Zahir, Mazyar, Zaki, Nazar, Zaman, Burhan Abdullah, Zangiabadian, Moein, Zare, Fariba, Zare, Iman, Zareshahrabadi, Zahra, Zarrintan, Armin, Zastrozhin, Mikhail Sergeevich, Zeineddine, Mohammad A.; Zhang, Dongyu, Zhang, Jianrong, Zhang, Yunquan, Zhang, Zhi-Jiang, Zhou, Linghui, Zodpey, Sanjay, Zoladl, Mohammad, Vos, Theo, Hay, Simon I.; Force, Lisa M.; Murray, Christopher J. L..
The Lancet ; 400(10352):563-591, 2022.
Article in English | ProQuest Central | ID: covidwho-1991370

ABSTRACT

Summary Background Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk–outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. Findings Globally, in 2019, the risk factors included in this analysis accounted for 4·45 million (95% uncertainty interval 4·01–4·94) deaths and 105 million (95·0–116) DALYs for both sexes combined, representing 44·4% (41·3–48·4) of all cancer deaths and 42·0% (39·1–45·6) of all DALYs. There were 2·88 million (2·60–3·18) risk-attributable cancer deaths in males (50·6% [47·8–54·1] of all male cancer deaths) and 1·58 million (1·36–1·84) risk-attributable cancer deaths in females (36·3% [32·5–41·3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20·4% (12·6–28·4) and DALYs by 16·8% (8·8–25·0), with the greatest percentage increase in metabolic risks (34·7% [27·9–42·8] and 33·3% [25·8–42·0]). Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Funding Bill & Melinda Gates Foundation.

2.
Bastard, Paul, Vazquez, Sara, Liu, Jamin, Laurie, Matthew T.; Wang, Chung Yu, Gervais, Adrian, Le Voyer, Tom, Bizien, Lucy, Zamecnik, Colin, Philippot, Quentin, Rosain, Jérémie, Catherinot, Emilie, Willmore, Andrew, Mitchell, Anthea M.; Bair, Rebecca, Garçon, Pierre, Kenney, Heather, Fekkar, Arnaud, Salagianni, Maria, Poulakou, Garyphallia, Siouti, Eleni, Sahanic, Sabina, Tancevski, Ivan, Weiss, Günter, Nagl, Laurenz, Manry, Jérémy, Duvlis, Sotirija, Arroyo-Sánchez, Daniel, Paz Artal, Estela, Rubio, Luis, Perani, Cristiano, Bezzi, Michela, Sottini, Alessandra, Quaresima, Virginia, Roussel, Lucie, Vinh, Donald C.; Reyes, Luis Felipe, Garzaro, Margaux, Hatipoglu, Nevin, Boutboul, David, Tandjaoui-Lambiotte, Yacine, Borghesi, Alessandro, Aliberti, Anna, Cassaniti, Irene, Venet, Fabienne, Monneret, Guillaume, Halwani, Rabih, Sharif-Askari, Narjes Saheb, Danielson, Jeffrey, Burrel, Sonia, Morbieu, Caroline, Stepanovskyy, Yurii, Bondarenko, Anastasia, Volokha, Alla, Boyarchuk, Oksana, Gagro, Alenka, Neuville, Mathilde, Neven, Bénédicte, Keles, Sevgi, Hernu, Romain, Bal, Antonin, Novelli, Antonio, Novelli, Giuseppe, Saker, Kahina, Ailioaie, Oana, Antolí, Arnau, Jeziorski, Eric, Rocamora-Blanch, Gemma, Teixeira, Carla, Delaunay, Clarisse, Lhuillier, Marine, Le Turnier, Paul, Zhang, Yu, Mahevas, Matthieu, Pan-Hammarström, Qiang, Abolhassani, Hassan, Bompoil, Thierry, Dorgham, Karim, consortium, Covid Hge, French, Covid study group, consortium, Comet, Gorochov, Guy, Laouenan, Cédric, Rodríguez-Gallego, Carlos, Ng, Lisa F. P.; Renia, Laurent, Pujol, Aurora, Belot, Alexandre, Raffi, François, Allende, Luis M.; Martinez-Picado, Javier, Ozcelik, Tayfun, Keles, Sevgi, Imberti, Luisa, Notarangelo, Luigi D.; Troya, Jesus, Solanich, Xavier, Zhang, Shen-Ying, Puel, Anne, Wilson, Michael R.; Trouillet-Assant, Sophie, Abel, Laurent, Jouanguy, Emmanuelle, Ye, Chun Jimmie, Cobat, Aurélie, Thompson, Leslie M.; Andreakos, Evangelos, Zhang, Qian, Anderson, Mark S.; Casanova, Jean-Laurent, DeRisi, Joseph L..
Science immunology ; 2022.
Article in English | EuropePMC | ID: covidwho-1918542

ABSTRACT

Life-threatening ‘breakthrough’ cases of critical COVID-19 are attributed to poor or waning antibody response to the SARS-CoV-2 vaccine in individuals already at risk. Pre-existing autoantibodies (auto-Abs) neutralizing type I IFNs underlie at least 15% of critical COVID-19 pneumonia cases in unvaccinated individuals;however, their contribution to hypoxemic breakthrough cases in vaccinated people remains unknown. Here, we studied a cohort of 48 individuals (age 20-86 years) who received 2 doses of an mRNA vaccine and developed a breakthrough infection with hypoxemic COVID-19 pneumonia 2 weeks to 4 months later. Antibody levels to the vaccine, neutralization of the virus, and auto-Abs to type I IFNs were measured in the plasma. Forty-two individuals had no known deficiency of B cell immunity and a normal antibody response to the vaccine. Among them, ten (24%) had auto-Abs neutralizing type I IFNs (aged 43-86 years). Eight of these ten patients had auto-Abs neutralizing both IFN-α2 and IFN-ω, while two neutralized IFN-ω only. No patient neutralized IFN-β. Seven neutralized 10 ng/mL of type I IFNs, and three 100 pg/mL only. Seven patients neutralized SARS-CoV-2 D614G and the Delta variant (B.1.617.2) efficiently, while one patient neutralized Delta slightly less efficiently. Two of the three patients neutralizing only 100 pg/mL of type I IFNs neutralized both D61G and Delta less efficiently. Despite two mRNA vaccine inoculations and the presence of circulating antibodies capable of neutralizing SARS-CoV-2, auto-Abs neutralizing type I IFNs may underlie a significant proportion of hypoxemic COVID-19 pneumonia cases, highlighting the importance of this particularly vulnerable population. Type I IFN auto-Abs are found in 20% of hypoxemic, mRNA vaccinated COVID-19 patients despite SARS-CoV-2 neutralizing antibodies. Description

3.
Acta Biochim Biophys Sin (Shanghai) ; 2022 Jun 25.
Article in English | MEDLINE | ID: covidwho-1903505

ABSTRACT

Clinical information on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in patients with inborn errors of immunity (IEI) during the current Coronavirus disease 2019 (COVID-19) pandemic is still limited. Proper DNA repair machinery is required for the development of the adaptive immune system, which provides specific and long-term protection against SARS-CoV-2. This review highlights the impact of SARS-CoV-2 infections on IEI patients with DNA repair disorders and summarizes susceptibility risk factors, pathogenic mechanisms, clinical manifestations and management strategies of COVID-19 in this special patient population.

4.
J Exp Med ; 219(8)2022 Aug 01.
Article in English | MEDLINE | ID: covidwho-1901005

ABSTRACT

Recessive or dominant inborn errors of type I interferon (IFN) immunity can underlie critical COVID-19 pneumonia in unvaccinated adults. The risk of COVID-19 pneumonia in unvaccinated children, which is much lower than in unvaccinated adults, remains unexplained. In an international cohort of 112 children (<16 yr old) hospitalized for COVID-19 pneumonia, we report 12 children (10.7%) aged 1.5-13 yr with critical (7 children), severe (3), and moderate (2) pneumonia and 4 of the 15 known clinically recessive and biochemically complete inborn errors of type I IFN immunity: X-linked recessive TLR7 deficiency (7 children) and autosomal recessive IFNAR1 (1), STAT2 (1), or TYK2 (3) deficiencies. Fibroblasts deficient for IFNAR1, STAT2, or TYK2 are highly vulnerable to SARS-CoV-2. These 15 deficiencies were not found in 1,224 children and adults with benign SARS-CoV-2 infection without pneumonia (P = 1.2 × 10-11) and with overlapping age, sex, consanguinity, and ethnicity characteristics. Recessive complete deficiencies of type I IFN immunity may underlie ∼10% of hospitalizations for COVID-19 pneumonia in children.


Subject(s)
COVID-19 , Interferon Type I , Pneumonia , Adult , COVID-19/genetics , Child , Humans , Inheritance Patterns , SARS-CoV-2
5.
JAMA Oncol ; 8(3): 420-444, 2022 Mar 01.
Article in English | MEDLINE | ID: covidwho-1664325

ABSTRACT

IMPORTANCE: The Global Burden of Diseases, Injuries, and Risk Factors Study 2019 (GBD 2019) provided systematic estimates of incidence, morbidity, and mortality to inform local and international efforts toward reducing cancer burden. OBJECTIVE: To estimate cancer burden and trends globally for 204 countries and territories and by Sociodemographic Index (SDI) quintiles from 2010 to 2019. EVIDENCE REVIEW: The GBD 2019 estimation methods were used to describe cancer incidence, mortality, years lived with disability, years of life lost, and disability-adjusted life years (DALYs) in 2019 and over the past decade. Estimates are also provided by quintiles of the SDI, a composite measure of educational attainment, income per capita, and total fertility rate for those younger than 25 years. Estimates include 95% uncertainty intervals (UIs). FINDINGS: In 2019, there were an estimated 23.6 million (95% UI, 22.2-24.9 million) new cancer cases (17.2 million when excluding nonmelanoma skin cancer) and 10.0 million (95% UI, 9.36-10.6 million) cancer deaths globally, with an estimated 250 million (235-264 million) DALYs due to cancer. Since 2010, these represented a 26.3% (95% UI, 20.3%-32.3%) increase in new cases, a 20.9% (95% UI, 14.2%-27.6%) increase in deaths, and a 16.0% (95% UI, 9.3%-22.8%) increase in DALYs. Among 22 groups of diseases and injuries in the GBD 2019 study, cancer was second only to cardiovascular diseases for the number of deaths, years of life lost, and DALYs globally in 2019. Cancer burden differed across SDI quintiles. The proportion of years lived with disability that contributed to DALYs increased with SDI, ranging from 1.4% (1.1%-1.8%) in the low SDI quintile to 5.7% (4.2%-7.1%) in the high SDI quintile. While the high SDI quintile had the highest number of new cases in 2019, the middle SDI quintile had the highest number of cancer deaths and DALYs. From 2010 to 2019, the largest percentage increase in the numbers of cases and deaths occurred in the low and low-middle SDI quintiles. CONCLUSIONS AND RELEVANCE: The results of this systematic analysis suggest that the global burden of cancer is substantial and growing, with burden differing by SDI. These results provide comprehensive and comparable estimates that can potentially inform efforts toward equitable cancer control around the world.


Subject(s)
Global Burden of Disease , Neoplasms , 50308 , Global Health , Humans , Incidence , Neoplasms/epidemiology , Prevalence , Quality-Adjusted Life Years , Risk Factors
6.
J Clin Immunol ; 42(3): 471-483, 2022 04.
Article in English | MEDLINE | ID: covidwho-1653615

ABSTRACT

BACKGROUND: Inborn errors of immunity (IEI) and autoantibodies to type I interferons (IFNs) underlie critical COVID-19 pneumonia in at least 15% of the patients, while the causes of multisystem inflammatory syndrome in children (MIS-C) remain elusive. OBJECTIVES: To detect causal genetic variants in very rare cases with concomitant critical COVID-19 pneumonia and MIS-C. METHODS: Whole exome sequencing was performed, and the impact of candidate gene variants was investigated. Plasma levels of cytokines, specific antibodies against the virus, and autoantibodies against type I IFNs were also measured. RESULTS: We report a 3-year-old child who died on day 56 of SARS-CoV-2 infection with an unusual clinical presentation, combining both critical COVID-19 pneumonia and MIS-C. We identified a large, homozygous loss-of-function deletion in IFNAR1, underlying autosomal recessive IFNAR1 deficiency. CONCLUSIONS: Our findings confirm that impaired type I IFN immunity can underlie critical COVID-19 pneumonia, while suggesting that it can also unexpectedly underlie concomitant MIS-C. Our report further raises the possibility that inherited or acquired dysregulation of type I IFN immunity might contribute to MIS-C in other patients.


Subject(s)
COVID-19 , Interferon Type I , Autoantibodies , COVID-19/complications , Child, Preschool , Cytokines , Humans , Receptor, Interferon alpha-beta/genetics , SARS-CoV-2 , Systemic Inflammatory Response Syndrome
7.
iScience ; 25(2): 103743, 2022 Feb 18.
Article in English | MEDLINE | ID: covidwho-1611783

ABSTRACT

Information concerning the longevity of immunity to SARS-CoV-2 following natural infection may have considerable implications for durability of immunity induced by vaccines. Here, we monitored the SARS-CoV-2 specific immune response in COVID-19 patients followed up to 15 months after symptoms onset. Following a peak at day 15-28 postinfection, the IgG antibody response and plasma neutralizing titers gradually decreased over time but stabilized after 6 months. Compared to G614, plasma neutralizing titers were more than 8-fold lower against variants Beta, Gamma, and Delta. SARS-CoV-2-specific memory B and T cells persisted in the majority of patients up to 15 months although a significant decrease in specific T cells, but not B cells, was observed between 6 and 15 months. Antiviral specific immunity, especially memory B cells in COVID-19 convalescent patients, is long-lasting, but some variants of concern may at least partially escape the neutralizing activity of plasma antibodies.

8.
Allergol Immunopathol (Madr) ; 49(6): 63-66, 2021.
Article in English | MEDLINE | ID: covidwho-1513272

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has affected millions of people around the world. This zoonotic-enveloped virus is primarily transmitted through inhalation. Infected people are commonly asymptomatic or manifest mild symptoms, including fever, cough, diarrhea, and fatigue. However, it may lead to severe patterns associated with multiple organ failure in individuals with an impaired immune system. OBJECTIVE: Here we report a 7-year-old girl with hyper-immunoglobulin M (IgM) (HIgM) phenotype, admitted to the hospital emergency department with fever, cough, and pneumonia symptoms because of the COVID-19 infection. Coronavirus infection was confirmed by a positive real-time polymerase chain reaction test. Surprisingly, serum levels of both IgG and IgA of the patient were transiently normalized during the COVID-19 infection when tested prior to the monthly injection of intravenous immunoglobulin. After she recovered from the COVID infection, her immunoglobulin levels returned to the primary stage and she demonstrated HIgM phenotype. CONCLUSION: Since this transient increase in the levels of immunoglobulins was solely observed during the COVID-19 infection, and no other infectious episodes were diagnosed in the patient, clarifying the exact cause would help to understand in a better manner the implications and specification of humoral immunity in patients with primary antibody deficiencies.


Subject(s)
COVID-19/complications , Hyper-IgM Immunodeficiency Syndrome/virology , Child , Female , Humans , Immunoglobulin M/blood
9.
J Clin Immunol ; 42(1): 1-9, 2022 01.
Article in English | MEDLINE | ID: covidwho-1482248

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) exhibits a wide spectrum of clinical manifestations, ranging from asymptomatic to critical conditions. Understanding the mechanism underlying life-threatening COVID-19 is instrumental for disease prevention and treatment in individuals with a high risk. OBJECTIVES: We aimed to identify the genetic cause for critical COVID-19 pneumonia in a patient with a preexisting inborn error of immunity (IEI). METHODS: Serum levels of specific antibodies against the virus and autoantibodies against type I interferons (IFNs) were measured. Whole exome sequencing was performed, and the impacts of candidate gene variants were investigated. We also evaluated 247 ataxia-telangiectasia (A-T) patients in the Iranian IEI registry. RESULTS: We report a 7-year-old Iranian boy with a preexisting hyper IgM syndrome who developed critical COVID-19 pneumonia. IgM only specific COVID-19 immune response was detected but no autoantibodies against type I IFN were observed. A homozygous deleterious mutation in the ATM gene was identified, which together with his antibody deficiency, radiosensitivity, and neurological signs, established a diagnosis of A-T. Among the 247 A-T patients evaluated, 36 had SARS-CoV-2 infection, but all had mild symptoms or were asymptomatic except the index patient. A hemizygous deleterious mutation in the TLR7 gene was subsequently identified in the patient. CONCLUSIONS: We report a unique IEI patient with combined ATM and TLR7 deficiencies. The two genetic defects underlie A-T and critical COVID-19 in this patient, respectively.


Subject(s)
Ataxia Telangiectasia/genetics , COVID-19/genetics , Pneumonia/genetics , Toll-Like Receptor 7/deficiency , Toll-Like Receptor 7/genetics , Child , Humans , Iran , Male
11.
Adv Exp Med Biol ; 1318: 91-107, 2021.
Article in English | MEDLINE | ID: covidwho-1222709

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes novel coronavirus disease (COVID-19), is the seventh pathogenic coronavirus recently discovered in December 2019 in Wuhan, China. To date, our knowledge about its effect on the human host remains limited. It is well known that host genetic factors account for the individual differences in the susceptibility to infectious diseases. The genetic susceptibility factors to COVID-19 and its severity are associated with several unanswered questions. However, the experience gained from an earlier strain of coronavirus, SARS-CoV-1, which shows 78% genetic similarity to SARS-CoV-2 and uses the same receptor to bind to host cells, could provide some clues. It, therefore, seems possible to assemble new evidence in order to solve a potential genetic predisposition puzzle for COVID-19. In this chapter, the puzzle pieces, including virus entry receptors, immune response, and inflammation-related genes, as well as the probable genetic predisposition models to COVID-19, are discussed.


Subject(s)
COVID-19 , Communicable Diseases , China/epidemiology , Genetic Predisposition to Disease , Humans , SARS-CoV-2
12.
Med (N Y) ; 2(3): 281-295.e4, 2021 03 12.
Article in English | MEDLINE | ID: covidwho-1078082

ABSTRACT

BACKGROUND: Monitoring the adaptive immune responses during the natural course of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection provides useful information for the development of vaccination strategies against this virus and its emerging variants. We thus profiled the serum anti-SARS-CoV-2 antibody (Ab) levels and specific memory B and T cell responses in convalescent coronavirus disease 2019 (COVID-19) patients. METHODS: A total of 119 samples from 88 convalescent donors who experienced mild to critical disease were tested for the presence of elevated anti-spike and anti-receptor binding domain Ab levels over a period of 8 months. In addition, the levels of SARS-CoV-2 neutralizing Abs and specific memory B and T cell responses were tested in a subset of samples. FINDINGS: Anti-SARS-CoV-2 Abs were present in 85% of the samples collected within 4 weeks after the onset of symptoms in COVID-19 patients. Levels of specific immunoglobulin M (IgM)/IgA Abs declined after 1 month, while levels of specific IgG Abs and plasma neutralizing activities remained relatively stable up to 6 months after diagnosis. Anti-SARS-CoV-2 IgG Abs were still present, although at a significantly lower level, in 80% of the samples collected at 6-8 months after symptom onset. SARS-CoV-2-specific memory B and T cell responses developed with time and were persistent in all of the patients followed up for 6-8 months. CONCLUSIONS: Our data suggest that protective adaptive immunity following natural infection of SARS-CoV-2 may persist for at least 6-8 months, regardless of disease severity. Development of medium- or long-term protective immunity through vaccination may thus be possible. FUNDING: This project was supported by the European Union's Horizon 2020 research and innovation programme (ATAC, no. 101003650), the Italian Ministry of Health (Ricerca Finalizzata grant no. GR-2013-02358399), the Center for Innovative Medicine, and the Swedish Research Council. J.A. was supported by the SciLifeLab/KAW national COVID-19 research program project grant 2020.


Subject(s)
COVID-19 , SARS-CoV-2 , Antibodies, Viral , Humans , Immunoglobulin A , Immunoglobulin G , T-Lymphocytes
13.
J Clin Immunol ; 41(2): 345-355, 2021 02.
Article in English | MEDLINE | ID: covidwho-954575

ABSTRACT

Although it is estimated that COVID-19 life-threatening conditions may be diagnosed in less than 1:1000 infected individuals below the age of 50, but the real impact of this pandemic on pediatric patients with different types of primary immunodeficiency (PID) is not elucidated. The current prospective study on a national registry of PID patients showed that with only 1.23 folds higher incidence of infections, these patients present a 10-folds higher mortality rate compared to population mainly in patients with combined immunodeficiency and immune dysregulation. Therefore, further management modalities against COVID-19 should be considered to improve the survival rate in these two PID entities using hematopoietic stem cell transplantation and immunomodulatory agents.


Subject(s)
COVID-19/complications , COVID-19/epidemiology , Health Impact Assessment , Primary Immunodeficiency Diseases/complications , Primary Immunodeficiency Diseases/epidemiology , SARS-CoV-2 , COVID-19/diagnosis , COVID-19/virology , Child, Preschool , Clinical Decision-Making , Comorbidity , Disease Management , Female , Humans , Infant , Male , Mortality , Primary Immunodeficiency Diseases/diagnosis , Public Health Surveillance , Severity of Illness Index
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