Following the severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), another highly pathogenic coronavirus named SARS-CoV-2 (previously known as 2019-nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS-CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical symptoms similar to those reported for SARS-CoV and MERS-CoV. The most characteristic symptom of patients with COVID-19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID-19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS-CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse-connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS-CoV and SARS-CoV2, it remains to make clear whether the potential invasion of SARS-CoV2 is partially responsible for the acute respiratory failure of patients with COVID-19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS-CoV-2-induced respiratory failure.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jmv.25728

The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients

The pathway by which semliki forest virus (SFV), a membrane-containing animal virus, enters BHK-21 cells was studied morphologically and biochemically. After attaching to the cell surface, the majority of viruses was rapidly trapped into coated pits, internalized by endocytosis in coated vesicles, and sequestered into intracellular vacuoles and lysosomes. Direct penetration of viruses through the plasma membrane was never observed. To assess the possible involvement of lysosomes in the release of the genome into the cytoplasm, the effect of five lysosomotropic agents, known to increase the lysosomal pH, was tested. All of these agents inhibited SFV infectivity and one, chloroquine (the agent studied in most detail), inhibited a very early step in the infection but had no effect on binding, endocytosis, or intracellular distribution of SFV. Thus, the inhibitory effect was concluded to be either on penetration of the nucelocapsid into the cytoplasm or on uncoating of the viral RNA. Possible mechanisms for the penetration of the genome into the cytoplasm were studied in vitro, using phospholipids-cholesterol liposomes and isolated SFV. When the pH was 6.0 or lower, efficient fusion of the viral membranes and the liposomal membranes occurred, resulting in the transfer of the nucleocapsid into the liposomes. Infection of cells could also be induced by brief low pH treatment of cells with bound SFV under conditions where the normal infection route was blocked. The results suggest that the penetration of the viral genome into the cytosol takes place intracellularly through fusion between the limiting membrane of intracellular vacuoles and the membrane of viruses contained within them. The low pH required for fusion together with the inhibitory effect of lysosomotropic agents implicate lysosomes, or other intracellular vacuoles with sufficiently low pH, as the main sites of penetration.

/pdf/on-the-entry-of-semliki-forest-virus-into-bhk-21-cells-2dy4tjqw3z.pdf

On the entry of Semliki Forest virus into BHK-21 cells.

This chapter describes the interactions between the different structural components of the viruses and discusses their relevance for the process of virion formation. Two key factors determine the efficiency of the assembly process: intracellular transport and molecular interactions. Many viruses have evolved elaborate strategies to ensure the swift and accurate delivery of the virion components to the cellular compartment(s) where they must meet and form (sub) structures. Assembly of viruses starts in the nucleus by the encapsidation of viral DNA, using cytoplasmically synthesized capsid proteins; nucleocapsids then migrate to the cytosol, by budding at the inner nuclear membrane followed by deenvelopment, to pick up the tegument proteins.

Molecular interactions in the assembly of coronaviruses.

Publisher Summary Coronaviruses have recently emerged as an important group of animal and human pathogens that share a distinctive replicative cycle. Some of the unique characteristics in the replication of coronaviruses include generation of a 3' coterminal-nested set of five or six subgenomic mRNAs, each of which appears to direct the synthesis of one protein. Two virus-specific RNA polymerase activities have been identified. Many of the distinctive features of coronavirus infection and coronavirus-induced diseases may result from the properties of the two coronavirus glycoproteins. The intracellular budding site, which may be important in the establishment and maintenance of persistent infections, appears to be due to the restricted intracytoplasmic migration of the E1 glycoprotein, which acts as a matrix-like transmembrane glycoprotein. E1 also exhibits distinctive behavior by self-aggregating on heating at 100°C in sodium dodecyl sulfate (SDS) and by its interaction with RNA in the viral nucleocapsid. The E1 of mouse hepatitis virus (MHV) is an O-linked glycoprotein, unlike most other viral glycoproteins. Thus, the coronavirus system may be a useful model for the study of synthesis, glycosylation, and transport of O-linked cellular glycoproteins.

The molecular biology of coronaviruses

Coronaviruses are frequently claimed to have a characteristic morphology, including the possession of a “club-shaped” surface projection or spike (S) glycoprotein However, in common with other aspects of the coronaviruses, the group exhibits variation with respect to the shape, size, and distribution of the S protein on the virion surface Davies and Macnaughton (1979) described the spikes of infectious bronchitis virus (IBV) and human coronavirus (HCV) 229E as being “tear-drop” shaped and widely spaced, whereas those of murine hepatitis virus (MHV) type 3 were mostly “cone-shaped” and closely spaced, although in some MHV-3 preparations the spikes were more bulbous Dimensions of S vary not only among the coronaviruses but also depending on the staining procedure; following potassium phosphotungstate staining all three viruses had spikes approximately 20 nm long and 10 nm wide at the bulbous end, except for the cone-shaped spikes of MHV, which had a diameter of only 5 nm (Davies and Macnaughton, 1979) The entire S protein has been observed after solubilization and purification (Sturman et al, 1980; Cavanagh, 1983c) The nonenvelope-associated S1 subunit of the IBV S protein can become detached from the virion (Stern and Sefton, 1982a; Cavanagh and Davis, 1986)

/pdf/the-coronavirus-surface-glycoprotein-2nblj5fsry.pdf

The Coronavirus Surface Glycoprotein

Primary chick kidney cells were infected with avian infectious bronchitis virus (IBV) and examined by electron microscopy. Virus particles entered the cells by viropexis and distinction could be made between engulfment by cell processes (phagocytosis) and entry by micropinocytosis in coated transport vesicles.

/pdf/morphogenesis-of-avian-infectious-bronchitis-virus-in-8rsoxnmhr5.pdf

Morphogenesis of avian infectious bronchitis virus in primary chick kidney cells.

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Morphogenesis of avian infectious bronchitis virus in primary chick kidney cells.