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J Med Virol ; 2020 Oct 01.
Article in English | MEDLINE | ID: covidwho-807875


The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a significant and urgent threat to global health. This review provided strong support for central nervous system (CNS) infection with SARS-CoV-2 and shed light on the neurological mechanism underlying the lethality of SARS-CoV-2 infection. Among the published data, only 1.28% COVID-19 patients who underwent cerebrospinal fluid (CSF) tests were positive for SARS-CoV-2 in CSF. However, this does not mean the absence of CNS infection in most COVID-19 patients because postmortem studies revealed that some patients with CNS infection showed negative results in CSF tests for SARS-CoV-2. Among 20 neuropathological studies reported so far, SARS-CoV-2 was detected in the brain of 58 cases in nine studies, and three studies have provided sufficient details on the CNS infection in COVID-19 patients. Almost all in vitro and in vivo experiments support the neuroinvasive potential of SARS-CoV-2. In infected animals, SARS-CoV-2 was found within neurons in different brain areas with a wide spectrum of neuropathology, consistent with the reported clinical symptoms in COVID-19 patients. Several lines of evidence indicate that SARS-CoV-2 used the hematopoietic route to enter the CNS. But more evidence supports the trans-neuronal hypothesis. SARS-CoV-2 has been found to invade the brain via the olfactory, gustatory, and trigeminal pathways, especially at the early stage of infection. Severe COVID-19 patients with neurological deficits are at a higher risk of mortality, and only the infected animals showing neurological symptoms became dead, suggesting that neurological involvement may be one cause of death.

Compr Psychiatry ; 102: 152202, 2020 10.
Article in English | MEDLINE | ID: covidwho-720480


OBJECTIVE: This study aimed to investigate the mental state of medical staff and medical students in the early stages of the SARS-CoV-2 outbreak, as well as analyze the risk factors of serious mental illness (SMI), so as to provide a scientific basis for further psychological intervention and management. METHOD: A cross-sectional survey was conducted from February 2-7, 2020. The Kessler 6 Psychological Distress Scale and a general information questionnaire were administered on-line to a convenience sample of 548 medical staff and medical students in China. Multivariate binary logistic regression analysis was used to screen the risk factors of SMI in medical staff and medical students. RESULTS: Of the 505 respondents in the final analysis, 188 (37.23%) were at high risk of SMI. Respondents were at significantly higher risk of SMI if they had been suspected of being infected with the SARS-CoV-2 (OR = 7.00, 95% CI: 1.19-41.14), had relatives suspected of being infected with the SARS-CoV-2 (OR = 23.60, 95% CI: 1.11-501.30), felt concerned towards media coverage of outbreak-related information (OR = 11.95, 95% CI: 3.07-46.57), recently dreamed related to SARS-CoV-2 (OR = 4.21, 95% CI: 2.22-8.01), experienced difficulty in controlling emotions during SARS-CoV-2 epidemic (OR = 3.25, 95% CI: 1.66-6.37), or spent hours watching outbreaks per day (OR = 1.29, 95% CI: 1.13-1.46). CONCLUSION: Our findings highlight that medical staff and medical students were vulnerable to SMI during the early stages of the SARS-CoV-2 outbreak and identify the factors associated with SMI which can be used to formulate psychological interventions to improve the mental health. The independent risk factors for SMI among them are suspicion that they or relatives were infected with the SARS-CoV-2, greater interest in media reports about the epidemic, frequency of recent dreams related to SARS-CoV-2, difficulty in controlling emotions during the epidemic, and hours spent watching outbreaks per day.

Coronavirus Infections/psychology , Health Personnel/psychology , Pneumonia, Viral/psychology , Students, Medical/psychology , Adult , Betacoronavirus , China/epidemiology , Coronavirus Infections/epidemiology , Cross-Sectional Studies , Disease Outbreaks , Female , Humans , Male , Mental Health , Pandemics , Pneumonia, Viral/epidemiology , Risk Factors , Surveys and Questionnaires
J Med Virol ; 2020 Jun 11.
Article in English | MEDLINE | ID: covidwho-593351


As compared to many other viral pulmonary infections, there existed several peculiar manifestations in the COVID-19 patients, including the "silence" of pneumonia in both mild and severe cases and a long intensive care unit stay for those requiring invasive mechanical ventilation. Similar silent pneumonia has been documented in the infectioninduced by H5N1 influenza virus HK483 and was found to result from the direct attack of the virus on the bronchopulmonary C-fibers at the early stage and the final infection in the brainstem at the late stage. The long stay of critical patients in the intensive care unit is possibly due to the depression of central respiratory drive, which resulted in the failure to wean from the mechanic ventilation. Carotid and aortic bodies and bronchopulmonary C-fibers are two key peripheral components responsible for the chemosensitive responses in the respiratory system, while triggering respiratory reflexes depends predominantly on the putative chemosensitive neurons located in the pontomedullary nuclei. In view of the findings for the H5N1 influenza virus, the silence of pneumonia induced by SARS-CoV-2 may be due to the possible impairment of peripheral chemosensitive reflexes as well as the damage to the respiratory-related central neurons.