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. 2020 May;35(5):716-720.
doi: 10.1002/mds.28084. Epub 2020 Apr 24.

SARS-CoV-2: At the Crossroad Between Aging and Neurodegeneration

Alice Lippi  1   2 , Renato Domingues  1 , Cristian Setz  1   3 , Tiago F Outeiro  1   4   5 , Anita Krisko  1
Affiliations

SARS-CoV-2: At the Crossroad Between Aging and Neurodegeneration

Alice Lippi et al. Mov Disord. 2020 May.
No abstract available

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Figures

Figure 1
Figure 1
Putative modus operandi of SARS‐CoV‐2. Upon binding to the angiotensin‐converting enzyme 2 (ACE2) receptor, the virus enters the host cells and hijacks the cellular machineries for its own replication, affecting pathways relevant in the maintenance of cellular longevity. The virus seizes control over the host's Hsp90 (yellow circles) to enhance the function of its RNA polymerase. Lysosomal activity (black circles) is inhibited, leading to protein aggregation in target cells, including neurons, thus increasing the long‐term likelihood of neurodegenerative diseases, such as PD. Viral ORF‐9b localizes to mitochondria, propelling mitochondrial dysfunction, as well as an overall turmoil of redox homeostasis. The viral spike protein enters the ER and activates the UPR, which, together with the inhibition of the ubiquitin‐proteasome system, leads to cell‐wide protein misfolding. This model is based on literature currently available on SARS‐CoV, SARS‐Cov‐2, and influenza A virus. [Color figure can be viewed at http://wileyonlinelibrary.com]
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