Special Issue: Coronaviruses and the Cytoskeleton

Note from the Editor:  How does SARS-CoV-2 enter and navigate host cells? While this complex process remains elusive for a number of human betacoronaviruses, published studies on related viruses may serve as a springboard for understanding the infection and pathogenicity of the novel coronavirus underlying COVID-19.  We have distilled a portion of the current literature below to support you in combating what is now a global pandemic.

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Tubulins interact with porcine and human S proteins of the genus Alphacoronavirus and support successful assembly and release of infectious viral particles
Rüdiger et al.  |  Virology  |  2016

• The cytoplasmic tail of Alphacoronavirus spike protein interacts with tubulin.
• Drug-induced microtubule depolymerization reduces virus titer.
• Microtubules may mediate the transport and assembly of spike proteins into virions during the coronavirus replication cycle.

COVID-19 UPDATE: Scientists prioritized resolving the structure of the novel coronavirus spike protein and have achieved a 3.5 A resolution by cryo-EM. Link in Science

Effect of microtubule disruption on neuronal spread and replication of demyelinating and nondemyelinating strains of mouse hepatitis virus in vitro
Biswas and Sarma  |  Journal of Virology  |  2014

• Spike proteins govern the microtubule-mediated transport of select murine coronaviruses.
• Microtubule disruption reduces virus titer in a dose-dependent manner.
• Microtubule-mediated axonal transport may be essential for viral replication and infection.

Ezrin interacts with the SARS coronavirus spike protein and restrains infection at the entry stage
Millet et al.  |  PLOS One  |  2012

• Ezrin, a membrane-actin linker, interacts with the spike protein of SARS-CoV.
• Ezrin functions as a physical constraint to limit SARS-CoV host cell entry.

Entry of human coronavirus NL63 into the cell
Milewska et al.  |  Journal of Virology  |  2018

• Human coronavirus NL63 remains immobilized at the cell surface upon actin stabilization.
• Actin depolymerizing agents similarly prevent viral internalization.
• Remodeling of the actin cortex is required for host cell infection by human coronavirus NL63.

COVID-19 UPDATE: Last week, scientists at Westlake University in Hangzhou, China, discovered that SARS-CoV-2 attaches to the same cell surface receptor as the NL63 virus, ACE2. Link in Science

Early events during human coronavirus OC43 entry to the cell
Owczarek et al.  |  Scientific Reports  |  2018

• The human coronavirus OC43 requires actin for internalization into host cells.
• OC43 is transported along the host actin cytoskeleton following entry by endocytosis.
• Actin depolymerization does not block internalization but does limit virus infection rate.

Interaction of the coronavirus infectious bronchitis virus membrane protein with β-actin and its implication in virion assembly and budding
Wang et al.  |  PLOS One  |  2009

• Actin interacts with the M protein from coronavirus infectious bronchitis virus.
• Disruption of the actin cytoskeleton with cytochalasin D hampers the release of virus particles.
• Actin may serve an essential function in the coronavirus replication cycle – including virion assembly and budding.

Our opinions are our own and do not represent the views or endorsement of the authors cited.