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iNature
Severe neurological symptoms are associated
with Coronavirus disease 2019 (COVID-19).
However, despite evidence of neurotropic infection, its morphological features, pathological nature, and underlying mechanisms in the patient's brain have not been revealed
.
On January 6, 2023, Bian Xiuwu of the University of Science and Technology of China/Army Medical University, Leng Ling of the Chinese Academy of Medical Sciences/Peking Union Medical College Hospital, and Ping Yifang and Yao Xiaohong of the Army Medical University published an online report entitled " COVID-19-associated monocytic encephalitis (CAME): histological and proteomic evidence from autopsy" research paper through systematic pathological and proteomic analysis of the COVID-19 autopsy brain, The deciminator profile of COVID-19-associated encephalitis with monocyte infiltration and glial cell activation was determined.
Monocytes infiltration and microglia activation suggest that they have the potential to be therapeutic targets for COVID-19
.
In summary, the results of this study identify the histopathological and molecular characteristics of COVID-19-associated monocytic encephalitis (CAME) and suggest potential therapeutic targets
.
caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) that causes multiple organ dysfunction syndromes (MODS).
The global pandemic has killed more than 6.
6 million people, especially among
older people with pre-existing lung and cardiovascular disease.
Although most people with COVID-19 present primarily with respiratory symptoms, it is increasingly recognized that people with COVID-19 have a wide range of neurological symptoms, manifestations, and complications
.
Major neurologic manifestations ranging from mild to severe include anxiety, depression, visual changes, impaired mobility, numbness, tremors, and myalgia in the extremities, as well as loss
of memory, hearing, taste, or smell.
The onset of acute mild and severe COVID-19 can be followed by a series of persistent symptoms, called "long crowns", which can affect multiple organs
, including the central nervous system.
Understanding the pathological nature and mechanisms of neurological manifestations is important
to improve the prognosis of COVID-19.
Previous reports of neuropathic changes in the brain of COVID-19 patients include microglial nodules, neurophagocytosis, neuronal damage, and endotheliitis
.
These changes are considered nonspecific due to ischemia, bleeding, inflammation, and aging
.
There have also been reports of damage
to microvascular structures in COVID-19 patients.
In a subset of patients, levels of several cytokines, such as interleukin-6, IL-8, IL-15, and macrophage inflammatory protein-1b (MIP-1b), are elevated and associated with disruption of the blood-brain barrier (BBB)25 Despite autopsy evidence to support encephalitis and/or meningoencephalitis in patients with COVID-19, However, a comprehensive analysis
of COVID-19-related brain inflammation and infiltration of immune cells has not been conducted.
Previous studies have shown that the brain tissue of COVID-19 patients may be infected with the SARS-CoV-2 virus
.
The neurotropic nature of the SARS-CoV-2 virus has been demonstrated
in mouse and organoid models.
It has been proposed that the SARS-CoV-2 virus enters the nervous system
via axonal or choroidal pathways.
However, the severity of neuropathic changes did not correlate
with viral load.
The detection of SARS-CoV-2 virus in the patient brain parenchyma, particularly neurons and glial cells, remains controversial
.
It is worth noting that severe neuropsychiatric manifestations do not match
minor pathological changes in the brain.
Other mechanisms, such as induced inflammatory and ischemic responses, and other comorbidities that may be involved in the pathogenesis of COVID-19 brain pathology, previously observed in 6 COVID-19 patients with pan-encephalitis associated with T lymphocyte infiltration, "massive intracranial area" and "diffuse spotting hemorrhage throughout the brain" have been questioned, and a better understanding of the molecular mechanisms of brain injury will help develop treatments
for this disease.
In this study, researchers quantitatively evaluated neuropathic damage and infiltration of inflammatory cells
in the postmortem brains of 9 severely ill patients with COVID-19 and 9 age-matched healthy individuals by immunohistochemical staining, electron microscopy ultrastructural examination, and image thresholds.
Identification of differentially expressed proteins
using quantitative proteomic methods.
Histopathology presents with nerve phagocytosis, microglial nodules, satellite phenomena, extensive oedema, focal haemorrhage, infarction, and monocytic infiltration
.
Figure 1.
COVID-19 brain monocytes infiltration and extensive microglial activation (Image from Signal Transduction and Targeted Therapy).
Further studies have shown that COVID-19 brain immunostaining shows extensive activation of microglia and astrocytes, severe damage to the blood–brain barrier (BBB), varying degrees of CD14+/CD16+/CD141+/CCR7+/CD11c+ monocytes around blood vessels, and occasionally CD4+/CD8+ T lymphocyte infiltration
。 Quantitative proteomic analysis combined with bioinformatics analysis found that the brains of COVID-19 patients were mainly involved in upregulated proteins
for immune response, autophagy, and cellular metabolism compared to the control group.
Brain development, neuroprotection, and downregulation of extracellular matrix protein expression in the basement membrane may be caused
by activation of transforming growth factor β receptors and vascular endothelial growth factor signaling pathways.
Figure 2.
Neuronal and myelin damage associated with abnormal protein expression in the COVID-19 brain (Image from Signal Transduction and Targeted Therapy) In summary, this study defines the neuropathological nature of the brain as COVID-19-associated monocytic encephalitis, which may be caused by aseptic perivascular and parenchymal inflammation, Endothelial cell infection with SARS-CoV-2, hypoxic-ischemic encephalopathy, and secondary infection with lung microorganisms
.
Over the past two years, several studies have reported brain damage
associated with COVID-19.
However, the existence and etiology of encephalitis/meningitis have been controversial
.
The previously reported diagnosis of COVID-19 meningitis and/or encephalitis relied on clinical manifestations such as neck stiffness, vomiting, CT and MRI images, and PCR testing of viral RNA in cerebrospinal fluid without pathological evidence until the original neuropathological findings of COVID-19 autopsy in the brain Controversial viral test results and unknown pathological nature of inflammation prompted further investigation of its mechanisms
.
These current results reveal the pathological nature
of COME with monocytic dominant encephalitis and microglial activation-mediated inflammatory damage.
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The content is [iNature]
