Emerging neurotropic features of SARS-CoV-2

Zhan, Wen-Rong; Huang, Jing; Zeng, Peng-Ming; Tian, Wei-Ya; Luo, Zhen-Ge

doi:10.1093/jmcb/mjab044

Cited by 13 publications

(12 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Neurological post-acute sequelae of SARS-CoV-2 infection (PASC) are common, although direct viral infection of the central nervous system (CNS) is rare [ 3 , 6 ]. Instead, inflammatory mechanisms, parenchymal hypoxia or microvascular injuries may contribute to the development of CNS injury, raising the possibility that these long-term symptoms may be accompanied by systemic biomarkers of neuronal damage or neuroinflammation.…”

mentioning

confidence: 99%

No serological evidence for neuronal damage or reactive gliosis in neuro-COVID-19 patients with long-term persistent headache

Boni

Odainic

Gancarczyk

et al. 2022

Neurol. Res. Pract.

View full text Add to dashboard Cite

Recent studies have indicated that long-term neurological sequelae after COVID-19 are not accompanied by an increase of canonical biomarkers of central nervous system injury in blood, but subgroup stratifications are lacking. This is a particular concern in chronic headache, which can be a leading symptom of Post-COVID diseases associated with neuronal damage such as vasculitis or autoimmune encephalitis. We here compared patients with mild Post-COVID-19 syndrome and persistent headache (persistent Post-COVID-19 headache) lasting longer than 12 weeks after the initial serological diagnosis, to patients with mild and severe COVID-19 and COVID-19-negative controls. Levels of neurofilament light chain and glial fibrillary astrocytic protein, i.e. markers of neuronal damage and reactive astrogliosis, were lower in blood from patients with persistent Post-COVID-19 headache compared to patients with severe COVID-19. Hence, our pilot serological study indicates that long-term Post-COVID-19 headache may not be a sign of underlying neuronal damage or neuroinflammation.

show abstract

mentioning

confidence: 99%

No serological evidence for neuronal damage or reactive gliosis in neuro-COVID-19 patients with long-term persistent headache

Boni

Odainic

Gancarczyk

et al. 2022

Neurol. Res. Pract.

View full text Add to dashboard Cite

show abstract

“…Despite the numerous reports on COVID-19, it is still debatable if SARS-CoV-2 invades the Central Nervous System (CNS) via olfactory neurons ( Brann et al, 2020 ) and infects neurons and glia of the CNS ( Zhan et al, 2021 ; Jacob et al, 2020 ; Song et al, 2021 ; Dobrindt et al, 2021 ; Pellegrini et al, 2020 ; Pedrosa et al, 2021 ; Wu et al, 2020b ; Yang et al, 2020 ). Different groups have shown that human neural progenitor cells, grown either as brain organoids or as neurospheres, are permissive to SARS-CoV-2 infection ( Song et al, 2021 ; Yang et al, 2020 ; Bullen et al, 2020 ; Ramani et al, 2020 ; Zhang et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 Permissive glioblastoma cell line for high throughput antiviral screening

et al. 2022

View full text Add to dashboard Cite

“…Despite the numerous reports on COVID-19, it is still debatable if SARS-CoV-2 invades the Central Nervous System (CNS) via olfactory neurons (27) and infects neurons and glia of the CNS (28)(29)(30)(31)(32)(33)(34)(35). Different groups have shown that human neural progenitor cells, grown either as brain organoids or as neurospheres, are permissive to SARS-CoV-2 infection (30,(35)(36)(37)(38).…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 Permissive Glioblastoma Cell Line for High Throughput Antiviral Screening

Vanhulle

Stroobants

Provinciael

et al. 2022

Preprint

View full text Add to dashboard Cite

Despite the great success of the administered vaccines against SARS-CoV-2, the virus can still spread, as evidenced by the current circulation of the highly contagious Omicron variant. This emphasizes the additional need to develop effective antiviral countermeasures. In the context of early preclinical studies for antiviral assessment, robust cellular infection systems are required to screen drug libraries. In this study, we reported the implementation of a human glioblastoma cell line, stably expressing ACE2, in a SARS-CoV-2 cytopathic effect (CPE) reduction assay. These glioblastoma cells, designated as U87.ACE2+, expressed ACE2 and cathepsin B abundantly, but had low cellular levels of TMPRSS2 and cathepsin L. The U87.ACE2+ cells fused highly efficiently and quickly with SARS-CoV-2 spike expressing cells. Furthermore, upon infection with SARS-CoV-2 wild-type virus, the U87.ACE2+ cells displayed rapidly a clear CPE that resulted in complete cell lysis and destruction of the cell monolayer. By means of several readouts we showed that the U87.ACE2+ cells actively replicate SARS-CoV-2. Interestingly, the U87.ACE2+ cells could be successfully implemented in an MTS-based colorimetric CPE reduction assay, providing IC50 values for Remdesivir in the low nanomolar range. Lastly, the U87.ACE2+ cells were consistently permissive to all tested SARS-CoV-2 variants of concern, including the current Omicron variant. Thus, ACE2 expressing glioblastoma cells are highly permissive to SARS-CoV-2 with productive viral replication and with the induction of a strong CPE that can be utilized in high-throughput screening platforms.

show abstract

Emerging neurotropic features of SARS-CoV-2

Cited by 13 publications

References 78 publications

No serological evidence for neuronal damage or reactive gliosis in neuro-COVID-19 patients with long-term persistent headache

No serological evidence for neuronal damage or reactive gliosis in neuro-COVID-19 patients with long-term persistent headache

SARS-CoV-2 Permissive glioblastoma cell line for high throughput antiviral screening

SARS-CoV-2 Permissive Glioblastoma Cell Line for High Throughput Antiviral Screening

Contact Info

Product

Resources

About