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Your search keyword '"Schulz, Wade L."' showing total 10 results
Start Over Author "Schulz, Wade L." Publisher springer science and business media llc
10 results on '"Schulz, Wade L."'

1. Evidence of leaky protection following COVID-19 vaccination and SARS-CoV-2 infection in an incarcerated population

Author

Lind, Margaret L., primary, Dorion, Murilo, additional, Houde, Amy J., additional, Lansing, Mary, additional, Lapidus, Sarah, additional, Thomas, Russell, additional, Yildirim, Inci, additional, Omer, Saad B., additional, Schulz, Wade L., additional, Andrews, Jason R., additional, Hitchings, Matt D. T., additional, Kennedy, Byron S., additional, Richeson, Robert P., additional, Cummings, Derek A. T., additional, and Ko, Albert I., additional

Published
2023
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4. De novo emergence of a remdesivir resistance mutation during treatment of persistent SARS-CoV-2 infection in an immunocompromised patient: a case report

Author

Gandhi, Shiv, primary, Klein, Jonathan, additional, Robertson, Alexander J., additional, Peña-Hernández, Mario A., additional, Lin, Michelle J., additional, Roychoudhury, Pavitra, additional, Lu, Peiwen, additional, Fournier, John, additional, Ferguson, David, additional, Mohamed Bakhash, Shah A. K., additional, Catherine Muenker, M., additional, Srivathsan, Ariktha, additional, Wunder, Elsio A., additional, Kerantzas, Nicholas, additional, Wang, Wenshuai, additional, Lindenbach, Brett, additional, Pyle, Anna, additional, Wilen, Craig B., additional, Ogbuagu, Onyema, additional, Greninger, Alexander L., additional, Iwasaki, Akiko, additional, Schulz, Wade L., additional, and Ko, Albert I., additional

Published
2022
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5. A multicenter evaluation of computable phenotyping approaches for SARS-CoV-2 infection and COVID-19 hospitalizations

Author

Khera, Rohan, primary, Mortazavi, Bobak J., additional, Sangha, Veer, additional, Warner, Frederick, additional, Patrick Young, H., additional, Ross, Joseph S., additional, Shah, Nilay D., additional, Theel, Elitza S., additional, Jenkinson, William G., additional, Knepper, Camille, additional, Wang, Karen, additional, Peaper, David, additional, Martinello, Richard A., additional, Brandt, Cynthia A., additional, Lin, Zhenqiu, additional, Ko, Albert I., additional, Krumholz, Harlan M., additional, Pollock, Benjamin D., additional, and Schulz, Wade L., additional

Published
2022
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6. Sex differences in immune responses that underlie COVID-19 disease outcomes

Author

Takahashi, Takehiro, Ellingson, Mallory K., Wong, Patrick, Israelow, Benjamin, Lucas, Carolina, Klein, Jon, Silva, Julio, Mao, Tianyang, Oh, Ji Eun, Tokuyama, Maria, Lu, Peiwen, Venkataraman, Arvind, Park, Annsea, Liu, Feimei, Meir, Amit, Sun, Jonathan, Wang, Eric Y., Casanovas-Massana, Arnau, Wyllie, Anne L., Vogels, Chantal B. F., Earnest, Rebecca, Lapidus, Sarah, Ott, Isabel M., Moore, Adam J., Anastasio, Kelly, Askenase, Michael H., Batsu, Maria, Beatty, Hannah, Bermejo, Santos, Bickerton, Sean, Brower, Kristina, Bucklin, Molly L., Cahill, Staci, Campbell, Melissa, Cao, Yiyun, Courchaine, Edward, Datta, Rupak, DeIuliis, Giuseppe, Geng, Bertie, Glick, Laura, Handoko, Ryan, Kalinich, Chaney, Khoury-Hanold, William, Kim, Daniel, Knaggs, Lynda, Kuang, Maxine, Kudo, Eriko, Lim, Joseph, Linehan, Melissa, Lu-Culligan, Alice, Malik, Amyn A., Martin, Anjelica, Matos, Irene, McDonald, David, Minasyan, Maksym, Mohanty, Subhasis, Muenker, M. Catherine, Naushad, Nida, Nelson, Allison, Nouws, Jessica, Nunez-Smith, Marcella, Obaid, Abeer, Ott, Isabel, Park, Hong-Jai, Peng, Xiaohua, Petrone, Mary, Prophet, Sarah, Rahming, Harold, Rice, Tyler, Rose, Kadi-Ann, Sewanan, Lorenzo, Sharma, Lokesh, Shepard, Denise, Silva, Erin, Simonov, Michael, Smolgovsky, Mikhail, Song, Eric, Sonnert, Nicole, Strong, Yvette, Todeasa, Codruta, Valdez, Jordan, Velazquez, Sofia, Vijayakumar, Pavithra, Wang, Haowei, Watkins, Annie, White, Elizabeth B., Yang, Yexin, Shaw, Albert, Fournier, John B., Odio, Camila D., Farhadian, Shelli, Dela Cruz, Charles, Grubaugh, Nathan D., Schulz, Wade L., Ring, Aaron M., Ko, Albert I., Omer, Saad B., and Iwasaki, Akiko

Subjects
0301 basic medicine, Multidisciplinary, Innate immune system, biology, business.industry, T cell, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, medicine.anatomical_structure, Immune system, Immunity, 030220 oncology & carcinogenesis, Immunology, biology.protein, Medicine, Antibody, business, Viral load, Sex characteristics, Cohort study
Abstract

There is increasing evidence that coronavirus disease 2019 (COVID-19) produces more severe symptoms and higher mortality among men than among women1-5. However, whether immune responses against severe acute respiratory syndrome coronavirus (SARS-CoV-2) differ between sexes, and whether such differences correlate with the sex difference in the disease course of COVID-19, is currently unknown. Here we examined sex differences in viral loads, SARS-CoV-2-specific antibody titres, plasma cytokines and blood-cell phenotyping in patients with moderate COVID-19 who had not received immunomodulatory medications. Male patients had higher plasma levels of innate immune cytokines such as IL-8 and IL-18 along with more robust induction of non-classical monocytes. By contrast, female patients had more robust T cell activation than male patients during SARS-CoV-2 infection. Notably, we found that a poor T cell response negatively correlated with patients' age and was associated with worse disease outcome in male patients, but not in female patients. By contrast, higher levels of innate immune cytokines were associated with worse disease progression in female patients, but not in male patients. These findings provide a possible explanation for the observed sex biases in COVID-19, and provide an important basis for the development of a sex-based approach to the treatment and care of male and female patients with COVID-19.

Published
2020

7. Reply to: A finding of sex similarities rather than differences in COVID-19 outcomes

Author

Takahashi, Takehiro, primary, Ellingson, Mallory K., additional, Wong, Patrick, additional, Israelow, Benjamin, additional, Lucas, Carolina, additional, Klein, Jon, additional, Silva, Julio, additional, Mao, Tianyang, additional, Oh, Ji Eun, additional, Tokuyama, Maria, additional, Lu, Peiwen, additional, Venkataraman, Arvind, additional, Park, Annsea, additional, Liu, Feimei, additional, Meir, Amit, additional, Sun, Jonathan, additional, Wang, Eric Y., additional, Casanovas-Massana, Arnau, additional, Wyllie, Anne L., additional, Vogels, Chantal B. F., additional, Earnest, Rebecca, additional, Lapidus, Sarah, additional, Ott, Isabel M., additional, Moore, Adam J., additional, Shaw, Albert, additional, Fournier, John B., additional, Odio, Camila D., additional, Farhadian, Shelli, additional, Dela Cruz, Charles, additional, Grubaugh, Nathan D., additional, Schulz, Wade L., additional, Ring, Aaron M., additional, Ko, Albert I., additional, Omer, Saad B., additional, and Iwasaki, Akiko, additional

Published
2021
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9. Longitudinal analyses reveal immunological misfiring in severe COVID-19

Author

Lucas, Carolina, Wong, Patrick, Klein, Jon, Castro, Tiago B. R., Silva, Julio, Sundaram, Maria, Ellingson, Mallory K., Mao, Tianyang, Oh, Ji Eun, Israelow, Benjamin, Takahashi, Takehiro, Tokuyama, Maria, Lu, Peiwen, Venkataraman, Arvind, Park, Annsea, Mohanty, Subhasis, Wang, Haowei, Wyllie, Anne L., Vogels, Chantal B. F., Earnest, Rebecca, Lapidus, Sarah, Ott, Isabel M., Moore, Adam J., Muenker, M. Catherine, Fournier, John B., Campbell, Melissa, Odio, Camila D., Casanovas-Massana, Arnau, Obaid, Abeer, Lu-Culligan, Alice, Nelson, Allison, Brito, Anderson, Nunez, Angela, Martin, Anjelica, Watkins, Annie, Geng, Bertie, Kalinich, Chaney, Harden, Christina, Todeasa, Codruta, Jensen, Cole, Kim, Daniel, McDonald, David, Shepard, Denise, Courchaine, Edward, White, Elizabeth B., Song, Eric, Silva, Erin, Kudo, Eriko, DeIuliis, Giuseppe, Rahming, Harold, Park, Hong-Jai, Matos, Irene, Nouws, Jessica, Valdez, Jordan, Fauver, Joseph, Lim, Joseph, Rose, Kadi-Ann, Anastasio, Kelly, Brower, Kristina, Glick, Laura, Sharma, Lokesh, Sewanan, Lorenzo, Knaggs, Lynda, Minasyan, Maksym, Batsu, Maria, Petrone, Mary, Kuang, Maxine, Nakahata, Maura, Linehan, Melissa, Askenase, Michael H., Simonov, Michael, Smolgovsky, Mikhail, Sonnert, Nicole, Naushad, Nida, Vijayakumar, Pavithra, Martinello, Rick, Datta, Rupak, Handoko, Ryan, Bermejo, Santos, Prophet, Sarah, Bickerton, Sean, Velazquez, Sofia, Alpert, Tara, Rice, Tyler, Khoury-Hanold, William, Peng, Xiaohua, Yang, Yexin, Cao, Yiyun, Strong, Yvette, Herbst, Roy, Shaw, Albert C., Medzhitov, Ruslan, Schulz, Wade L., Grubaugh, Nathan D., Dela Cruz, Charles, Farhadian, Shelli, Ko, Albert I., Omer, Saad B., and Iwasaki, Akiko

Subjects
Adult, Male, 0301 basic medicine, Chemokine, T-Lymphocytes, medicine.medical_treatment, T cell, Pneumonia, Viral, Disease, Article, Pathogenesis, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Immune system, Cluster Analysis, Humans, Medicine, Pandemics, Aged, Aged, 80 and over, Interleukin-13, Innate immune system, Multidisciplinary, biology, business.industry, COVID-19, Immunoglobulin E, Middle Aged, Viral Load, Eosinophils, 030104 developmental biology, Cytokine, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Interleukin 13, Immunology, biology.protein, Cytokines, Female, Interleukin-5, Coronavirus Infections, business
Abstract

Recent studies have provided insights into the pathogenesis of coronavirus disease 2019 (COVID-19)1–4. However, the longitudinal immunological correlates of disease outcome remain unclear. Here we serially analysed immune responses in 113 patients with moderate or severe COVID-19. Immune profiling revealed an overall increase in innate cell lineages, with a concomitant reduction in T cell number. An early elevation in cytokine levels was associated with worse disease outcomes. Following an early increase in cytokines, patients with moderate COVID-19 displayed a progressive reduction in type 1 (antiviral) and type 3 (antifungal) responses. By contrast, patients with severe COVID-19 maintained these elevated responses throughout the course of the disease. Moreover, severe COVID-19 was accompanied by an increase in multiple type 2 (anti-helminths) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosinophils. Unsupervised clustering analysis identified four immune signatures, representing growth factors (A), type-2/3 cytokines (B), mixed type-1/2/3 cytokines (C), and chemokines (D) that correlated with three distinct disease trajectories. The immune profiles of patients who recovered from moderate COVID-19 were enriched in tissue reparative growth factor signature A, whereas the profiles of those with who developed severe disease had elevated levels of all four signatures. Thus, we have identified a maladapted immune response profile associated with severe COVID-19 and poor clinical outcome, as well as early immune signatures that correlate with divergent disease trajectories.

Published
2020
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