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.
Need a refresher on how viruses hijack cells?
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.