Abstract
To get access to the replication site, small non-enveloped DNA viruses have to cross the cell membrane using a limited number of capsid proteins, which also protect the viral genome in the extracellular environment. Most of DNA viruses have to reach the nucleus to replicate. The capsid proteins involved in transmembrane penetration are exposed or released during endosomal trafficking of the virus. Subsequently, the conserved domains of capsid proteins interact with cellular membranes and ensure their efficient permeabilization. This review summarizes our current knowledge concerning the role of capsid proteins of small non-enveloped DNA viruses in intracellular membrane perturbation in the early stages of infection.
Highlights
Viruses are cellular parasites that usurp the host cell energy and mechanisms for their own propagation
Adeno-associated viruses (AAVs) use VP3 as a major coat protein, which represents about 85% of total capsid proteins [61]
The results suggest that parvovirus needs low pH as an inducer of conformational changes of the capsid proteins
Summary
Viruses are cellular parasites that usurp the host cell energy and mechanisms for their own propagation The first barrier they have to overcome at the cellular level is the plasmatic membrane. The capsids of small non-enveloped DNA viruses can be described as very efficient gene vectors Understanding this step of infection, which is often rate-limiting, will help to design efficient gene vectors, applicable to various medical purposes. The current knowledge concerning the role of small non-enveloped DNA virus capsid proteins in overcoming the membrane barrier during early phases of infection is the subject of this review. We compared four viral families described in detail in this paper—Adenoviridae, Papillomaviridae, Polyomaviridae, and Parvoviridae These viruses share similarities in their “design”, and they overcome the same obstacles using similar weapons.
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