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1.
Emerg Microbes Infect ; 11(1): 1115-1125, 2022 Dec.
Article in English | MEDLINE | ID: covidwho-1799501

ABSTRACT

Diabetes mellitus (DM) is one of the most common underlying diseases that may aggravates COVID-19. In the present study, we explored islet function, the presence of SARS-CoV-2 and pathological changes in the pancreas of patients with COVID-19. Oral glucose tolerance tests (OGTTs) and the C-peptide release test demonstrated a decrease in glucose-stimulated C-peptide secretory capacity and an increase in HbA1c levels in patients with COVID-19. The prediabetic conditions appeared to be more significant in the severe group than in the moderate group. SARS-CoV-2 receptors (ACE2, CD147, TMPRSS2 and neuropilin-1) were expressed in pancreatic tissue. In addition to SARS-CoV-2 virus spike protein and virus RNA, coronavirus-like particles were present in the autophagolysosomes of pancreatic acinar cells of a patient with COVID-19. Furthermore, the expression and distribution of various proteins in pancreatic islets of patients with COVID-19 were altered. These data suggest that SARS-CoV-2 in the pancreas may directly or indirectly impair islet function.


Subject(s)
COVID-19 , Diabetes Mellitus , C-Peptide/metabolism , Diabetes Mellitus/metabolism , Humans , Pancreas , SARS-CoV-2
3.
Nat Commun ; 12(1): 2506, 2021 05 04.
Article in English | MEDLINE | ID: covidwho-1216457

ABSTRACT

It is unclear whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can directly infect human kidney, thus leading to acute kidney injury (AKI). Here, we perform a retrospective analysis of clinical parameters from 85 patients with laboratory-confirmed coronavirus disease 2019 (COVID-19); moreover, kidney histopathology from six additional COVID-19 patients with post-mortem examinations was performed. We find that 27% (23/85) of patients exhibited AKI. The elderly patients and cases with comorbidities (hypertension and heart failure) are more prone to develop AKI. Haematoxylin & eosin staining shows that the kidneys from COVID-19 autopsies have moderate to severe tubular damage. In situ hybridization assays illustrate that viral RNA accumulates in tubules. Immunohistochemistry shows nucleocapsid and spike protein deposits in the tubules, and immunofluorescence double staining shows that both antigens are restricted to the angiotensin converting enzyme-II-positive tubules. SARS-CoV-2 infection triggers the expression of hypoxic damage-associated molecules, including DP2 and prostaglandin D synthase in infected tubules. Moreover, it enhances CD68+ macrophages infiltration into the tubulointerstitium, and complement C5b-9 deposition on tubules is also observed. These results suggest that SARS-CoV-2 directly infects human kidney to mediate tubular pathogenesis and AKI.


Subject(s)
Acute Kidney Injury/etiology , COVID-19/complications , Kidney Tubules/virology , SARS-CoV-2/pathogenicity , Acute Kidney Injury/epidemiology , Acute Kidney Injury/pathology , Acute Kidney Injury/virology , Adult , Aged , Aged, 80 and over , Angiotensin-Converting Enzyme 2/metabolism , Antigens, Viral/genetics , Antigens, Viral/metabolism , COVID-19/epidemiology , COVID-19/virology , China/epidemiology , Female , Humans , Immunity, Innate , Kidney Function Tests , Kidney Tubules/metabolism , Kidney Tubules/pathology , Male , Middle Aged , Pandemics , Retrospective Studies , SARS-CoV-2/genetics , SARS-CoV-2/isolation & purification , Viral Proteins/genetics , Viral Proteins/metabolism , Young Adult
4.
Natl Sci Rev ; 7(12): 1868-1878, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-1087785

ABSTRACT

Systematic autopsy and comprehensive pathological analyses of COVID-19 decedents should provide insights into the disease characteristics and facilitate the development of novel therapeutics. In this study, we report the autopsy findings from the lungs and lymphatic organs of 12 COVID-19 decedents-findings that evaluated histopathological changes, immune cell signature and inflammatory factor expression in the lungs, spleen and lymph nodes. Here we show that the major pulmonary alterations included diffuse alveolar damage, interstitial fibrosis and exudative inflammation featured with extensive serous and fibrin exudates, macrophage infiltration and abundant production of inflammatory factors (IL-6, IP-10, TNFα and IL-1ß). The spleen and hilar lymph nodes contained lesions with tissue structure disruption and immune cell dysregulation, including lymphopenia and macrophage accumulation. These findings provide pathological evidence that links injuries of the lungs and lymphatic organs with the fatal systematic respiratory and immune malfunction in critically ill COVID-19 patients.

5.
Am J Forensic Med Pathol ; 42(2): 164-169, 2021 Jun 01.
Article in English | MEDLINE | ID: covidwho-1035550

ABSTRACT

ABSTRACT: As of August 23, 2020, the 2019 novel coronavirus disease (COVID-19) has infected more than 23,518,340 people and caused more than 810,492 deaths worldwide including 4,717 deaths in China. We present a case of a 53-year-old woman who was admitted to the hospital because of dry coughs and high fever on January 26, 2020, in Wuhan, China. She was not tested for SARS-CoV-2 RNA until on hospital day 11 (illness day 21) because of a significant shortage of test kits at the local hospital. Then, her test was positive for COVID-19 on hospital day 20. Despite intensive medical treatments, she developed respiratory failure with secondary bacterial infection and expired on hospital day 23 (3 days after she was tested positive for SARS-CoV-2 RNA). A systemic autopsy examination, including immunohistochemistry and ultrastructural studies, demonstrates that SARS-CoV-2 can infect multiple organs with profound adverse effect on the immune system, and the lung pathology is characterized by diffuse alveolar damage. Extrapulmonary SARS-CoV-2 RNA was detected in several organs postmortem. The detailed pathological features are described. In addition, this report highlights the value of forensic autopsy in studying SARS-CoV-2 infection and the importance of clinicopathological correlation in better understanding the pathogenesis of COVID-19.


Subject(s)
COVID-19/diagnosis , Autopsy , Epiglottitis/pathology , Female , Fibroblasts/pathology , Humans , Infarction/pathology , Intracranial Thrombosis/pathology , Kidney/blood supply , Kidney/pathology , Lung/pathology , Lymph Nodes/pathology , Lymphocytes/pathology , Middle Aged , Myocytes, Cardiac/pathology , Myofibroblasts/pathology , Necrosis , RNA, Viral/analysis , Splenic Infarction/pathology , Subarachnoid Hemorrhage/pathology , Thromboembolism/pathology , Thrombosis/pathology , Thyroiditis, Autoimmune/pathology , Urinary Bladder/pathology
6.
Curr Med Sci ; 40(4): 618-624, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-695581

ABSTRACT

The COVID-19 pandemic caused by SARS-CoV2 is characterized by a remarkable variation in clinical severity ranging from a mild illness to a fatal multi-organ disease. Understanding the dysregulated human immune responses in the fatal subjects is critical for management of COVID-19 patients and the pandemic. In this study, we examined the immune cell compositions in the lung tissues and hilar lymph nodes using immunohistochemistry on 6 deceased COVID-19 patients and 4 focal organizing pneumonia (FOP) patients who underwent lung surgery and served as controls. We found a dominant presence of macrophages and a general deficiency of T cells and B cells in the lung tissues from deceased COVID-19 patients. In contrast to the FOP patients, Tfh cells and germinal center formation were largely absent in the draining hilar lymph nodes in the deceased COVID-19 patients. This was correlated with reduced IgM and IgG levels compared to convalescent COVID-19 patients. In summary, our data highlight a defect of germinal center structure in deceased COVID-19 patients leading to an impaired humoral immunity. Understanding the mechanisms of this deficiency will be one of the key points for the management of this epidemic.


Subject(s)
Betacoronavirus , Coronavirus Infections/immunology , Germinal Center/immunology , Pneumonia, Viral/immunology , T-Lymphocytes, Helper-Inducer/immunology , Adaptive Immunity , Aged , Aged, 80 and over , COVID-19 , Case-Control Studies , China/epidemiology , Coronavirus Infections/mortality , Coronavirus Infections/pathology , Fatal Outcome , Female , Germinal Center/pathology , Humans , Lymphopenia/immunology , Lymphopenia/mortality , Lymphopenia/pathology , Macrophages/immunology , Macrophages/pathology , Male , Middle Aged , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/pathology , SARS-CoV-2 , T-Lymphocytes, Helper-Inducer/pathology
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