Brain, behavior, and immunity
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Brain Behav. Immun. · Jul 2020
ReviewNervous system involvement after infection with COVID-19 and other coronaviruses.
Viral infections have detrimental impacts on neurological functions, and even to cause severe neurological damage. Very recently, coronaviruses (CoV), especially severe acute respiratory syndrome CoV 2 (SARS-CoV-2), exhibit neurotropic properties and may also cause neurological diseases. ⋯ The pathobiology of these neuroinvasive viruses is still incompletely known, and it is therefore important to explore the impact of CoV infections on the nervous system. Here, we review the research into neurological complications in CoV infections and the possible mechanisms of damage to the nervous system.
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Brain Behav. Immun. · Jul 2020
ReviewAre we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms.
The coronavirus disease 19 (COVID-19) pandemic is a significant psychological stressor in addition to its tremendous impact on every facet of individuals' lives and organizations in virtually all social and economic sectors worldwide. Fear of illness and uncertainty about the future precipitate anxiety- and stress-related disorders, and several groups have rightfully called for the creation and dissemination of robust mental health screening and treatment programs for the general public and front-line healthcare workers. However, in addition to pandemic-associated psychological distress, the direct effects of the virus itself (several acute respiratory syndrome coronavirus; SARS-CoV-2), and the subsequent host immunologic response, on the human central nervous system (CNS) and related outcomes are unknown. ⋯ Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes, may accompany acute viral infection, or may follow infection by weeks, months, or longer in recovered patients. The potential mechanisms are also discussed, including viral and immunological underpinnings. Therefore, prospective neuropsychiatric monitoring of individuals exposed to SARS-CoV-2 at various points in the life course, as well as their neuroimmune status, are needed to fully understand the long-term impact of COVID-19, and to establish a framework for integrating psychoneuroimmunology into epidemiologic studies of pandemics.
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Brain Behav. Immun. · Jul 2020
LetterAt the height of the storm: Healthcare staff's health conditions and job satisfaction and their associated predictors during the epidemic peak of COVID-19.
This study reports the physical health, mental health, anxiety, depression, distress, and job satisfaction of healthcare staff in Iran when the country faced its highest number of total active COVID-19 cases. In a sample of 304 healthcare staff (doctors, nurses, radiologists, technicians, etc.), we found a sizable portion reached the cutoff levels of disorders in anxiety (28.0%), depression (30.6%), and distress (20.1%). ⋯ The predictors were also different from those identified in previous studies of healthcare staff during the COVID-19 crisis in China. This study helps to identify the healthcare staff in need to enable more targeted help as healthcare staff in many countries are facing peaks in their COVID-19 cases.
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Brain Behav. Immun. · Jul 2020
Toll-like receptor 7 contributes to neuropathic pain by activating NF-κB in primary sensory neurons.
Toll like receptor 7 (TLR7) is expressed in neurons of the dorsal root ganglion (DRG), but whether it contributes to neuropathic pain is elusive. We found that peripheral nerve injury caused by ligation of the fourth lumbar (L4) spinal nerve (SNL) or chronic constriction injury of sciatic nerve led to a significant increase in the expression of TLR7 at mRNA and protein levels in mouse injured DRG. Blocking this increase through microinjection of the adeno-associated virus (AAV) 5 expressing TLR7 shRNA into the ipsilateral L4 DRG alleviated the SNL-induced mechanical, thermal and cold pain hypersensitivities in both male and female mice. ⋯ Mechanistically, the increased TLR7 activated the NF-κB signaling pathway through promoting the translocation of p65 into the nucleus and phosphorylation of p65 in the nucleus from the injured DRG neurons. Our findings suggest that DRG TLR7 contributes to neuropathic pain by activating NF-κB in primary sensory neurons. TLR7 may be a potential target for therapeutic treatment of this disorder.
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Brain Behav. Immun. · Jul 2020
Letter Case ReportsGuillain-Barré syndrome as a complication of SARS-CoV-2 infection.