Role of Microtubule Motor Proteins in Adenoviral Infections
type: CreativeWork
description: Viruses have been described as a piece of nucleic acid surrounded by bad news. These bad news determine host specificity, pathogenicity, and virulence. In the case of adenovirus, a non-enveloped double-stranded DNA virus that causes self-limiting disease in healthy individuals but can cause severe and even fatal infection in immunocompromised patients, the bad news can be reduced to the viral capsid. The adenoviral capsid mainly consists of three proteins (fiber, penton base, hexon) that form a rigid shell to protect the viral genome outside of host cells. However, they are able to orchestrate a precise disassembly program initiated once the next susceptible cell is reached, leading to step-wise virus entry, controlled capsid disintegration, efficient DNA delivery, and production of progeny virus. Understanding adenovirus entry is not only beneficial for pathogenic but also therapeutic reasons since adenoviruses have become an increasingly popular vaccine and gene transfer vector due to their ability to infect a large array of dividing and post-mitotic cells, their large DNA capacity, and easy amplification. Attachment to cell surface receptors leads to cellular signaling events, some of which regulate receptor-mediated uptake into clathrin-coated pits. Conditions inside the endosome trigger escape of the virions from the organelle through membrane disruption 5-15 min post-infection and most capsids gain access to the nucleus about 30-45 min thereafter. Interestingly, adenovirus relies on the microtubule (MT) network, MT-dependent motor proteins, and virus-stimulated cAMP-activated kinase (protein kinase A, PKA) activity to traverse the cytoplasm during the critical intracellular transport phase between endosomal escape and nuclear pore complex attachment. The main virus transporter is the MT minus-end directed motor protein complex cytoplasmic dynein, which functions in organelle positioning, cell migration, cell division, and cell differentiation in uninfected cel…
abstract: Viruses have been described as a piece of nucleic acid surrounded by bad news. These bad news determine host specificity, pathogenicity, and virulence. In the case of adenovirus, a non-enveloped double-stranded DNA virus that causes self-limiting disease in healthy individuals but can cause severe and even fatal infection in immunocompromised patients, the bad news can be reduced to the viral capsid. The adenoviral capsid mainly consists of three proteins (fiber, penton base, hexon) that form a rigid shell to protect the viral genome outside of host cells. However, they are able to orchestrate a precise disassembly program initiated once the next susceptible cell is reached, leading to step-wise virus entry, controlled capsid disintegration, efficient DNA delivery, and production of progeny virus. Understanding adenovirus entry is not only beneficial for pathogenic but also therapeutic reasons since adenoviruses have become an increasingly popular vaccine and gene transfer vector due to their ability to infect a large array of dividing and post-mitotic cells, their large DNA capacity, and easy amplification. Attachment to cell surface receptors leads to cellular signaling events, some of which regulate receptor-mediated uptake into clathrin-coated pits. Conditions inside the endosome trigger escape of the virions from the organelle through membrane disruption 5-15 min post-infection and most capsids gain access to the nucleus about 30-45 min thereafter. Interestingly, adenovirus relies on the microtubule (MT) network, MT-dependent motor proteins, and virus-stimulated cAMP-activated kinase (protein kinase A, PKA) activity to traverse the cytoplasm during the critical intracellular transport phase between endosomal escape and nuclear pore complex attachment. The main virus transporter is the MT minus-end directed motor protein complex cytoplasmic dynein, which functions in organelle positioning, cell migration, cell division, and cell differentiation in uninfected cel…
author: Scherer, Julian
language: English
keywords: Biology, Adenoviruses, Double-stranded RNA, Phosphorylation, Kinesin, Microtubules, Hippocampus (Brain), Neurons
date published: 2013
date modified: 2026-07-24T01:44:25Z
provider: Columbia University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Columbia University

PropertyValue
property ID: DOI
value: 10.7916/D80C52W6