Special Issue "The Cell Biology of Coronavirus Infection"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 15 September 2020.

Special Issue Editor

Prof. Carolyn Machamer
Website
Guest Editor
Department of Cell Biology, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, 105 WBSB, Baltimore, MD 21205, USA

Special Issue Information

Dear Colleagues,

Coronaviruses are enveloped positive strand RNA viruses that infect mammals and birds. They have the interesting property of assembling at intracellular membranes. About 20% of common colds in humans are caused by coronaviruses. More severe diseases, including severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), are caused by novel coronaviruses that emerged from animal sources. Another novel coronavirus related to SARS coronavirus (SARS CoV-2) emerged in December 2019 and has spread globally, with significant mortality and economic impact. Much progress has been made in understanding the infectious diseases caused by human coronaviruses since the emergence of SARS and MERS. The animal sources, epidemiology, and types of infections have been well documented. However, there are still no approved vaccines or antiviral therapeutics for any human coronavirus infection.

This lack of treatment is due in part to an incomplete understanding of the basic biology of this family of viruses. Of particular interest is the unknown advantage of intracellular assembly and mechanism of virus egress from infected cells. These characteristics are potential untapped avenues for novel antiviral strategies. In this Special Issue of Cells, coronavirus infection will be examined from a cell biological perspective. Potential topics include virus entry, formation of replication organelles, genome replication and production of viral mRNA, synthesis and targeting of viral proteins, and assembly and budding in the endoplasmic reticulum-Golgi intermediate compartment and virion egress. How cells respond to coronavirus infection is another important potential topic, including how interferon-stimulated genes impact infection.

Prof. Carolyn Machamer
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • coronavirus
  • SARS
  • MERS
  • COVID-19
  • membrane fusion
  • intracellular assembly
  • Golgi complex
  • replication organelle
  • egress
  • host cell response

Published Papers (3 papers)

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Research

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Open AccessArticle
Host Gene Expression of Macrophages in Response to Feline Coronavirus Infection
Cells 2020, 9(6), 1431; https://doi.org/10.3390/cells9061431 - 09 Jun 2020
Abstract
Feline coronavirus is a highly contagious virus potentially resulting in feline infectious peritonitis (FIP), while the pathogenesis of FIP remains not well understood, particularly in the events leading to the disease. A predominant theory is that the pathogenic FIPV arises from a mutation, [...] Read more.
Feline coronavirus is a highly contagious virus potentially resulting in feline infectious peritonitis (FIP), while the pathogenesis of FIP remains not well understood, particularly in the events leading to the disease. A predominant theory is that the pathogenic FIPV arises from a mutation, so that it could replicate not only in enterocytes of the intestines but also in monocytes, subsequently systemically transporting the virus. The immune status and genetics of affected cats certainly play an important role in the pathogenesis. Considering the importance of genetics and host immune responses in viral infections, the goal of this study was to elucidate host gene expression in macrophages using RNA sequencing. Macrophages from healthy male cats infected with FIPV 79-1146 ex vivo displayed a differential host gene expression. Despite the virus uptake, aligned viral reads did not increase from 2 to 17 h. The overlap of host gene expression among macrophages from different cats was limited, even though viral transcripts were detected in the cells. Interestingly, some of the downregulated genes in all macrophages were involved in immune signaling, while some upregulated genes common for all cats were found to be inhibiting immune activation. Our results highlight individual host responses playing an important role, consistent with the fact that few cats develop feline infectious peritonitis despite a common presence of enteric FCoV. Full article
(This article belongs to the Special Issue The Cell Biology of Coronavirus Infection)
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Review

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Open AccessReview
Canonical and Noncanonical Autophagy as Potential Targets for COVID-19
Cells 2020, 9(7), 1619; https://doi.org/10.3390/cells9071619 - 05 Jul 2020
Abstract
The SARS-CoV-2 pandemic necessitates a review of the molecular mechanisms underlying cellular infection by coronaviruses, in order to identify potential therapeutic targets against the associated new disease (COVID-19). Previous studies on its counterparts prove a complex and concomitant interaction between coronaviruses and autophagy. [...] Read more.
The SARS-CoV-2 pandemic necessitates a review of the molecular mechanisms underlying cellular infection by coronaviruses, in order to identify potential therapeutic targets against the associated new disease (COVID-19). Previous studies on its counterparts prove a complex and concomitant interaction between coronaviruses and autophagy. The precise manipulation of this pathway allows these viruses to exploit the autophagy molecular machinery while avoiding its protective apoptotic drift and cellular innate immune responses. In turn, the maneuverability margins of such hijacking appear to be so narrow that the modulation of the autophagy, regardless of whether using inducers or inhibitors (many of which are FDA-approved for the treatment of other diseases), is usually detrimental to viral replication, including SARS-CoV-2. Recent discoveries indicate that these interactions stretch into the still poorly explored noncanonical autophagy pathway, which might play a substantial role in coronavirus replication. Still, some potential therapeutic targets within this pathway, such as RAB9 and its interacting proteins, look promising considering current knowledge. Thus, the combinatory treatment of COVID-19 with drugs affecting both canonical and noncanonical autophagy pathways may be a turning point in the fight against this and other viral infections, which may also imply beneficial prospects of long-term protection. Full article
(This article belongs to the Special Issue The Cell Biology of Coronavirus Infection)
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Open AccessReview
Vasculopathy and Coagulopathy Associated with SARS-CoV-2 Infection
Cells 2020, 9(7), 1583; https://doi.org/10.3390/cells9071583 - 30 Jun 2020
Abstract
The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in >500,000 deaths worldwide, including >125,000 deaths in the U.S. since its emergence in late December 2019 and June 2020. Neither curative anti-viral [...] Read more.
The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in >500,000 deaths worldwide, including >125,000 deaths in the U.S. since its emergence in late December 2019 and June 2020. Neither curative anti-viral drugs nor a protective vaccine is currently available for the treatment and prevention of COVID-19. Recently, new clinical syndromes associated with coagulopathy and vasculopathy have emerged as a cause of sudden death and other serious clinical manifestations in younger patients infected with SARS-CoV-2 infection. Angiotensin converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 and other coronaviruses, is a transmembrane protein expressed by lung alveolar epithelial cells, enterocytes, and vascular endothelial cells, whose physiologic role is to induce the maturation of angiotensin I to generate angiotensin 1-7, a peptide hormone that controls vasoconstriction and blood pressure. In this review, we provide the general context of the molecular and cellular mechanisms of SARS-CoV-2 infection with a focus on endothelial cells, describe the vasculopathy and coagulopathy syndromes in patients with SARS-CoV-2, and outline current understanding of the underlying mechanistic aspects. Full article
(This article belongs to the Special Issue The Cell Biology of Coronavirus Infection)
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