Bp distance tables port to port pro v.2.0

b Viral load in CNS tissues from SARS-CoV-2-inoculated rhesus macaques. Monkeys were observed for clinical signs, including body temperature, body weight, sample collection, chest radiograph, and necropsies as indicated.

Five rhesus monkeys (3вЂ“5 years old) were intranasally inoculated with 1вЂ‰Г—вЂ‰10 7 PFU of SARS-CoV-2 in 1вЂ‰mL PBS. a Scheme of the experimental design of intranasal SARS-CoV-2 inoculation. SARS-CoV-2 invades the CNS in rhesus monkeys post intranasal inoculation. 10 To our knowledge, this is the first experimental evidence of SARS-CoV-2 neuroinvasion in the NHP model, which provides important insights into the CNS-related pathogenesis of SARS-CoV-2. The data suggested that SARS-CoV-2 could be trafficked to the brain possibility via the olfactory route and caused the upregulation of neuroinflammatory factors, as reported by K18-hACE2 mice model. The infection of SARS-CoV-2 induced the inflammation possibly by targeting neurons, microglia, and astrocytes in the CNS in vivo and in vitro. We showed that SARS-CoV-2 RNA was detectable in the nasal mucosa, olfactory trigone, and the entorhinal area in chronological order. Therefore, in this study we used the established rhesus monkey model of COVID-19 to further address the invasion of SARS-CoV-2 to the CNS, including the possible route and the pathogenesis. SARS-CoV-2 neurotropism, the route of invading the CNS, and the distribution of the virus are essential for the diagnosis, prognosis, and intervention of COVID-19. However, there is limited information about the neurotropism of SARS-CoV-2 and replication ability in the CNS. 21вЂ“ 23 These models provide an effective means to study the neurological complications associated with SARS-CoV-2 infection. It was reported that intranasal inoculation with SARS-CoV-2 results in an acute lung injury in NHPs, associated with high levels of inflammatory cytokines and accumulation of immune cells in the lung. Non-human primate (NHP) models can recapitulate several aspects of human disease, which is crucial to understand the pathogenic processes involved in SARS-CoV-2 infection and the development of vaccines and antivirals. 10 Due to the limitation of CNS specimens of COVID-19 patients, it is difficult to fully elucidate SARS-CoV-2-induced neurological diseases. Such an entry route was proved to be possible in K18-hACE2 mice following intranasal inoculation of SARS-CoV-2. In addition, brains from autopsied COVID-19 patients showed SARS-CoV-2 invasion and replication in both the olfactory bulb and hypothalamus, 7, 19, 20 indicating that SARS-CoV-2 may invade to CNS via the olfactory route in some individuals. Intranasally 17 or intracranially 18 inoculated SARS-CoV has been detected throughout the brains of hACE2 transgenic mice, implying that SARS-CoV-2 may use olfactory neurons as the major access to the CNS. The known neurotropic viruses generally enter the CNS through olfactory neurons, with subsequent transneuronal spread to other sites of the CNS. 11 These results indicate that the nasal epithelium could be the portal site of the initial SARS-CoV-2 infection. 16 In both symptomatic and asymptomatic COVID-19 patients, nasal swabs have yielded higher viral loads than throat swabs. 14, 15 These two key factors for SARS-CoV-2 infection are highly expressed in nasal goblet cells and ciliary cells.

12, 13 SARS-CoV-2 enters host cells using the receptor ACE2 and transmembrane serine protease 2 (TMPRSS2) as same as SARS-CoV. 11 Most ОІ-CoVs have a neuroinvasive propensity.

SARS-CoV-2 belongs to the same ОІ coronavirus (ОІ-CoV) genus as SARS-CoV first reported in 2003, and they share approximately 80% genomic homology. 8вЂ“ 10 These evidences implicate that SARS-CoV-2 potentially invades the central nervous system (CNS) of COVID-19 patients and causes the neurological complications. SARS-CoV-2 viral particles have been found in the frontal lobe and cerebrospinal fluid (CSF) of COVID-19 patients, 3, 7 and SARS-CoV-2 replication can be detectable in the brains of human angiotensin-converting enzyme 2 (hACE2) knock-in mice. 5 The duration of insomnia symptoms is longer than that of fever, 6 suggesting that SARS-CoV-2 infection could lead to neurological damages.

4 Additionally, some COVID-19 patients show neurologic signs, such as headache, dizziness, nausea, anosmia, and ageusia. 2 In the COVID-19 patients, SARS-CoV-2 infection is accompanied by neurological complications, such as encephalitis 3 and acute polyradiculitis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in December 2019 1 and have caused the global pandemic of the acute and highly contagious coronavirus disease 2019 (COVID-19).

Bp distance tables port to port pro v.2.0