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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.

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. [ABSTRACT FROM AUTHOR]

• DNA and several RNA viruses demand access to the cell nucleus for replication. • The nuclear envelope (NE) is a critical barrier for viral entry and egress. • Viral entry occurs via nuclear pores, by awaiting NE breakdown or NE remodelling. • Nuclear pores, parapore transport and NE destabilization are used for viral egress. • Insights into nuclear bypass pathways can reveal new antiviral therapeutic strategies. Viruses are obligatory intracellular parasites. For their efficient replication, many require access to the nuclear interior. Yet, only few viral particles are small enough to passively diffuse through the nuclear pore complexes, calling for alternative strategies to bypass the nuclear envelope barrier. Some viruses will await mitotic nuclear envelope breakdown to gain access, whereas others will exploit more active means, for instance by hijacking nuclear pore transport or by directly targeting constituents of the nuclear envelope so as to remodel and temporarily perturb its integrity. After replication, newly produced viral DNA complexes need to cross the same barrier to exit the nucleus and enter the cytoplasm, where the final stages of virion maturation take place. There are also different flavours to the feat of nuclear egress that vary in delicacy and intensity. In this review, we define the major entry and egress strategies that are exploited by different viruses and describe the molecular details thereof. Ultimately, a deeper understanding of these pathways may help identifying molecular targets for blocking viral reproduction or spreading. [ABSTRACT FROM AUTHOR]