Special Issue "Cell-Host Interplay for Viral Nuclear Import"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (30 September 2021).

Special Issue Editor

Dr. Francesca Di Nunzio
E-Mail Website
Guest Editor
Department of Virology, VMV, Institut Pasteur, Paris, France
Interests: HIV; viral nuclear import; nuclear organization; nuclear pore complex

Special Issue Information

Dear Colleagues,

Access to the nuclear environment offers numerous benefits for viral replication and persistence. During viral infection, self-defense mechanisms are activated in the host cells to survive in response to viral invasion. Many of these mechanisms interfere with the viral journey towards the nucleus. However, viruses have evolved divergent strategies to evade an antiviral innate immunity response and to penetrate the nuclear compartment to deliver their genome. Most of them hijack the nuclear pore complex (NPC) of post-mitotic cells to reach the host nuclear environment. Usually, the nuclear entry step represents the bottleneck for the replication of many viruses due to the large size of their capsid. To counteract this steric obstacle, viruses evolved intriguing and fascinating strategies to cross the NPC to reach the host nucleus to generate new progeny. Those viruses establish an interplay between their own proteins and host factors to control the outcome of infection. Increasing the understanding of these processes will trigger the design of new drug strategies to tackle host–pathogen interactions for viral cures. Of note, in recent years, cutting-edge technologies have begun to shed light on the mechanisms underlying the viral nuclear entry. This Special Issue will overview mechanisms of nuclear import developed by viruses to invade the host.

Dr. Francesca Di Nunzio
Guest Editor

Manuscript Submission Information

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Keywords

  • viruses
  • nuclear import
  • host-viral interactions
  • nuclear pore and nuclear dynamics

Published Papers (5 papers)

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Review

Review
The Role of Capsid in HIV-1 Nuclear Entry
Viruses 2021, 13(8), 1425; https://0-doi-org.brum.beds.ac.uk/10.3390/v13081425 - 22 Jul 2021
Cited by 1 | Viewed by 668
Abstract
HIV-1 can infect non-dividing cells. The nuclear envelope therefore represents a barrier that HIV-1 must traverse in order to gain access to the host cell chromatin for integration. Hence, nuclear entry is a critical step in the early stages of HIV-1 replication. Following [...] Read more.
HIV-1 can infect non-dividing cells. The nuclear envelope therefore represents a barrier that HIV-1 must traverse in order to gain access to the host cell chromatin for integration. Hence, nuclear entry is a critical step in the early stages of HIV-1 replication. Following membrane fusion, the viral capsid (CA) lattice, which forms the outer face of the retroviral core, makes numerous interactions with cellular proteins that orchestrate the progress of HIV-1 through the replication cycle. The ability of CA to interact with nuclear pore proteins and other host factors around the nuclear pore determines whether nuclear entry occurs. Uncoating, the process by which the CA lattice opens and/or disassembles, is another critical step that must occur prior to integration. Both early and delayed uncoating have detrimental effects on viral infectivity. How uncoating relates to nuclear entry is currently hotly debated. Recent technological advances have led to intense discussions about the timing, location, and requirements for uncoating and have prompted the field to consider alternative uncoating scenarios that presently focus on uncoating at the nuclear pore and within the nuclear compartment. This review describes recent advances in the study of HIV-1 nuclear entry, outlines the interactions of the retroviral CA protein, and discusses the challenges of investigating HIV-1 uncoating. Full article
(This article belongs to the Special Issue Cell-Host Interplay for Viral Nuclear Import)
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Review
The Viral Capsid: A Master Key to Access the Host Nucleus
Viruses 2021, 13(6), 1178; https://0-doi-org.brum.beds.ac.uk/10.3390/v13061178 - 20 Jun 2021
Cited by 1 | Viewed by 1052
Abstract
Viruses are pathogens that have evolved to hijack the cellular machinery to replicate themselves and spread to new cells. During the course of evolution, viruses developed different strategies to overcome the cellular defenses and create new progeny. Among them, some RNA and many [...] Read more.
Viruses are pathogens that have evolved to hijack the cellular machinery to replicate themselves and spread to new cells. During the course of evolution, viruses developed different strategies to overcome the cellular defenses and create new progeny. Among them, some RNA and many DNA viruses require access to the nucleus to replicate their genome. In non-dividing cells, viruses can only access the nucleus through the nuclear pore complex (NPC). Therefore, viruses have developed strategies to usurp the nuclear transport machinery and gain access to the nucleus. The majority of these viruses use the capsid to manipulate the nuclear import machinery. However, the particular tactics employed by each virus to reach the host chromatin compartment are very different. Nevertheless, they all require some degree of capsid remodeling. Recent notions on the interplay between the viral capsid and cellular factors shine new light on the quest for the nuclear entry step and for the fate of these viruses. In this review, we describe the main components and function of nuclear transport machinery. Next, we discuss selected examples of RNA and DNA viruses (HBV, HSV, adenovirus, and HIV) that remodel their capsid as part of their strategies to access the nucleus and to replicate. Full article
(This article belongs to the Special Issue Cell-Host Interplay for Viral Nuclear Import)
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Review
Role of Transportin-SR2 in HIV-1 Nuclear Import
Viruses 2021, 13(5), 829; https://0-doi-org.brum.beds.ac.uk/10.3390/v13050829 - 04 May 2021
Cited by 1 | Viewed by 886
Abstract
The HIV replication cycle depends on the interaction of viral proteins with proteins of the host. Unraveling host–pathogen interactions during the infection is of great importance for understanding the pathogenesis and the development of antiviral therapies. To date HIV uncoating and nuclear import [...] Read more.
The HIV replication cycle depends on the interaction of viral proteins with proteins of the host. Unraveling host–pathogen interactions during the infection is of great importance for understanding the pathogenesis and the development of antiviral therapies. To date HIV uncoating and nuclear import are the most debated steps of the HIV-1 replication cycle. Despite numerous studies during past decades, there is still much controversy with respect to the identity and the role of viral and host factors involved in these processes. In this review, we provide a comprehensive overview on the role of transportin-SR2 as a host cell factor during active nuclear transport. Full article
(This article belongs to the Special Issue Cell-Host Interplay for Viral Nuclear Import)
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Review
Early Steps of Hepatitis B Life Cycle: From Capsid Nuclear Import to cccDNA Formation
Viruses 2021, 13(5), 757; https://0-doi-org.brum.beds.ac.uk/10.3390/v13050757 - 26 Apr 2021
Cited by 1 | Viewed by 997
Abstract
Hepatitis B virus (HBV) remains a major public health concern, with more than 250 million chronically infected people who are at high risk of developing liver diseases, including cirrhosis and hepatocellular carcinoma. Although antiviral treatments efficiently control virus replication and improve liver function, [...] Read more.
Hepatitis B virus (HBV) remains a major public health concern, with more than 250 million chronically infected people who are at high risk of developing liver diseases, including cirrhosis and hepatocellular carcinoma. Although antiviral treatments efficiently control virus replication and improve liver function, they cannot cure HBV infection. Viral persistence is due to the maintenance of the viral circular episomal DNA, called covalently closed circular DNA (cccDNA), in the nuclei of infected cells. cccDNA not only resists antiviral therapies, but also escapes innate antiviral surveillance. This viral DNA intermediate plays a central role in HBV replication, as cccDNA is the template for the transcription of all viral RNAs, including pregenomic RNA (pgRNA), which in turn feeds the formation of cccDNA through a step of reverse transcription. The establishment and/or expression of cccDNA is thus a prime target for the eradication of HBV. In this review, we provide an update on the current knowledge on the initial steps of HBV infection, from the nuclear import of the nucleocapsid to the formation of the cccDNA. Full article
(This article belongs to the Special Issue Cell-Host Interplay for Viral Nuclear Import)
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Review
The Nuclear Pore Complex Is a Key Target of Viral Proteases to Promote Viral Replication
Viruses 2021, 13(4), 706; https://0-doi-org.brum.beds.ac.uk/10.3390/v13040706 - 19 Apr 2021
Cited by 1 | Viewed by 697
Abstract
Various viruses alter nuclear pore complex (NPC) integrity to access the nuclear content favoring their replication. Alteration of the nuclear pore complex has been observed not only in viruses that replicate in the nucleus but also in viruses with a cytoplasmic replicative cycle. [...] Read more.
Various viruses alter nuclear pore complex (NPC) integrity to access the nuclear content favoring their replication. Alteration of the nuclear pore complex has been observed not only in viruses that replicate in the nucleus but also in viruses with a cytoplasmic replicative cycle. In this last case, the alteration of the NPC can reduce the transport of transcription factors involved in the immune response or mRNA maturation, or inhibit the transport of mRNA from the nucleus to the cytoplasm, favoring the translation of viral mRNAs or allowing access to nuclear factors necessary for viral replication. In most cases, the alteration of the NPC is mediated by viral proteins, being the viral proteases, one of the most critical groups of viral proteins that regulate these nucleus–cytoplasmic transport changes. This review focuses on the description and discussion of the role of viral proteases in the modification of nucleus–cytoplasmic transport in viruses with cytoplasmic replicative cycles and its repercussions in viral replication. Full article
(This article belongs to the Special Issue Cell-Host Interplay for Viral Nuclear Import)
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