Rui Liu1, Li Zhao2, Xiaoming Cheng3, Huan Han1, Cong Li2, Dong Li1, Andrew Liu4, Guosheng Gao5, Feng Zhou6, Fang Liu7, Yingan Jiang8, Chengliang Zhu1, Yuchen Xia2. 1. Department of Clinical Laboratory, Renmin Hospital of Wuhan University, Wuhan, China. 2. State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, Institute of Medical Virology, School of Basic Medical Sciences, Wuhan University, Wuhan, China. 3. Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. 4. Frank H. Netter MD School of Medicine, Quinnipiac University, North Haven, CT, USA. 5. Department of Clinical Laboratory, HwaMei Hospital, University of Chinese Academy of Sciences, Ningbo, China. 6. Hubei Clinical Center and Key Laboratory for Intestinal and Colorectal Diseases, Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, China. 7. State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, China. 8. Department of Infectious Diseases, Renmin Hospital, Wuhan University, Wuhan, China.
Abstract
BACKGROUND & AIMS: The outbreak of coronavirus disease 2019 (COVID-19) has been declared a pandemic. Although COVID-19 is caused by infection in the respiratory tract, extrapulmonary manifestations including dysregulation of the immune system and hepatic injury have been observed. Given the high prevalence of hepatitis B virus (HBV) infection in China, we sought to study the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and HBV coinfection in patients. METHODS: Blood samples of 50 SARS-CoV-2 and HBV coinfected patients, 56 SARS-CoV-2 mono-infected patients, 57 HBeAg-negative chronic HBV patient controls and 57 healthy controls admitted to Renmin Hospital of Wuhan University were collected in this study. Complete blood count and serum biochemistry panels including markers indicative of liver functions were performed. Cytokines including IFN-γ, TNF-α, IL-2, IL-4, IL-6 and IL-10 were evaluated. T cell, B cell and NK cell counts were measured using flow cytometry. RESULTS: SARS-CoV-2 and HBV coinfection did not significantly affect the outcome of the COVID-19. However, at the onset of COVID-19, SARS-CoV-2 and HBV coinfected patients showed more severe monocytopenia and thrombocytopenia as well as more disturbed hepatic function in albumin production and lipid metabolism. Most of the disarrangement could be reversed after recovery from COVID-19. CONCLUSIONS: While chronic HBV infection did not predispose COVID-19 patients to more severe outcomes, our data suggest SARS-CoV-2 and HBV coinfection poses a higher extent of dysregulation of host functions at the onset of COVID-19. Thus, caution needs to be taken with the management of SARS-CoV-2 and HBV coinfected patients.
BACKGROUND & AIMS: The outbreak of coronavirus disease 2019 (COVID-19) has been declared a pandemic. Although COVID-19 is caused by infection in the respiratory tract, extrapulmonary manifestations including dysregulation of the immune system and hepatic injury have been observed. Given the high prevalence of hepatitis B virus (HBV) infection in China, we sought to study the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and HBV coinfection in patients. METHODS: Blood samples of 50 SARS-CoV-2 and HBV coinfected patients, 56 SARS-CoV-2 mono-infectedpatients, 57 HBeAg-negative chronic HBVpatient controls and 57 healthy controls admitted to Renmin Hospital of Wuhan University were collected in this study. Complete blood count and serum biochemistry panels including markers indicative of liver functions were performed. Cytokines including IFN-γ, TNF-α, IL-2, IL-4, IL-6 and IL-10 were evaluated. T cell, B cell and NK cell counts were measured using flow cytometry. RESULTS:SARS-CoV-2 and HBV coinfection did not significantly affect the outcome of the COVID-19. However, at the onset of COVID-19, SARS-CoV-2 and HBV coinfected patients showed more severe monocytopenia and thrombocytopenia as well as more disturbed hepatic function in albumin production and lipid metabolism. Most of the disarrangement could be reversed after recovery from COVID-19. CONCLUSIONS: While chronic HBV infection did not predispose COVID-19patients to more severe outcomes, our data suggest SARS-CoV-2 and HBV coinfection poses a higher extent of dysregulation of host functions at the onset of COVID-19. Thus, caution needs to be taken with the management of SARS-CoV-2 and HBV coinfected patients.
Authors: Brit Long; Brandon M Carius; Summer Chavez; Stephen Y Liang; William J Brady; Alex Koyfman; Michael Gottlieb Journal: Am J Emerg Med Date: 2022-01-21 Impact factor: 4.093
Authors: Marco Spadaccini; Lorenzo Canziani; Alessio Aghemo; Ana Lleo; Roberta Maselli; Andrea Anderloni; Silvia Carrara; Alessandro Fugazza; Gaia Pellegatta; Piera Alessia Galtieri; Cesare Hassan; David Greenwald; Mark Pochapin; Michael Wallace; Prateek Sharma; Thomas Roesch; Pradeep Bhandari; Fabian Emura; Gottumukkala S Raju; Alessandro Repici Journal: United European Gastroenterol J Date: 2021-06-08 Impact factor: 6.866