Abstract
The ability of a virus to spread between individuals, its replication capacity and the clinical course of the infection are macroscopic consequences of a multifaceted molecular interaction of viral components with the host cell. The heavy impact of COVID-19 on the world population, economics and sanitary systems calls for therapeutic and prophylactic solutions that require a deep characterization of the interactions occurring between virus and host cells. Unveiling how SARS-CoV-2 engages with host factors throughout its life cycle is therefore fundamental to understand the pathogenic mechanisms underlying the viral infection and to design antiviral therapies and prophylactic strategies. Two years into the SARS-CoV-2 pandemic, this review provides an overview of the interplay between SARS-CoV-2 and the host cell, with focus on the machinery and compartments pivotal for virus replication and the antiviral cellular response. Starting with the interaction with the cell surface, following the virus replicative cycle through the characterization of the entry pathways, the survival and replication in the cytoplasm, to the mechanisms of egress from the infected cell, this review unravels the complex network of interactions between SARS-CoV-2 and the host cell, highlighting the knowledge that has the potential to set the basis for the development of innovative antiviral strategies.
Highlights
The Emergence of SARS-CoV-2In December 2019 several cases of an atypical viral respiratory infection, later named COVID-19, emerged in Wuhan, China [1]
If from one side it appears that the interaction between SARSCoV-2 proteins and unfolded protein response (UPR) effectors leads to the activation of this stress response, another recent article suggests that, even though CoVs infection initiate endoplasmic reticulum (ER) stress signaling and induces UPR components at the mRNA level, these are inhibited at the protein level [278]
As we have described earlier, SARSCoV-2 non-structural protein 1 (Nsp1) binds to the 40S subunit of the ribosome and shuts off host RNA translation [304], a mechanism that was observed in other coronaviruses including SARS-CoV [reviewed in [214, 305]], and which limits the ability of the host cells to express antiviral activities
Summary
In December 2019 several cases of an atypical viral respiratory infection, later named COVID-19, emerged in Wuhan, China [1]. SARS-CoV-2 is an enveloped, single-stranded positive-sense RNA virus with a diameter of 60–140 nm and spikes of 9– 12 nm in length (Figure 1). It is part of the betacoronavirus genus, which includes MERS-CoV and SARS-CoV [24]. The virus particle is made of structural viral proteins including spike (S), envelope (E), membrane (M), and nucleocapsid (N) protein (Figure 1 and Table 1). The virion contains a positive-sense, single-stranded RNA genome (+ssRNA) enclosed by a lipidic envelope and by structural viral proteins. Other proteins are inserted in the lipid envelope: the spike trimers (S), the envelope (E), and membrane (M) proteins
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