in which host cell organelle virus trying to reach
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To trigger infection, a virus binds to receptors on a host cell's plasma membrane. ... In nonproductive infection, the virus may be targeted to and trapped in organelles unsupportive of viral membrane fusion or penetration, events which normally enable the viral nucleic acid access to the host cytosol or nucleus.
To cause infection, a virus enters a host cell, replicates, and assembles, with the resulting new viral progeny typically released into the extracellular environment to initiate a new infection round. Virus entry, replication, and assembly are dynamic and coordinated processes that require precise interactions with host components, often within and surrounding a defined subcellular compartment. Accumulating evidence pinpoints the endoplasmic reticulum (ER) as a crucial organelle supporting viral entry, replication, and assembly. This review focuses on the molecular mechanism by which different viruses co-opt the ER to accomplish these crucial infection steps. Certain bacterial toxins also hijack the ER for entry. An interdisciplinary approach, using rigorous biochemical and cell biological assays coupled with advanced microscopy strategies, will push to the next level our understanding of the virus-ER interaction during infection.
To trigger infection, a virus binds to receptors on a host cell’s plasma membrane. This interaction induces virus internalization, and initiates a complex journey of the viral particle into the host’s interior that leads to either nonproductive or productive infection (Mercer et al. 2010). In nonproductive infection, the virus may be targeted to and trapped in organelles unsupportive of viral membrane fusion or penetration, events which normally enable the viral nucleic acid access to the host cytosol or nucleus. Alternatively, the virus could be transported to a degradative intracellular compartment in which it is destroyed. In contrast, for productive infection, a viral particle must avoid these nonproductive routes and traffic along a pathway that allows it to reach the appropriate replication and assembly site. Successful infection is usually completed when the newly assembled particle is released into the extracellular milieu, in which it can promote another infection round. Thus, the ability to co-opt a host cell entry pathway leading to efficient replication and assembly ultimately dictates the fate of an incoming virus.
For proper entry, replication, and assembly, viruses often rely on the complex membranous network surrounding and residing within the host cell, such as the plasma, endolysosomal, and endoplasmic reticulum (ER) membranes. Selecting the suitable membrane system requires several considerations. To support entry, the membranous system must possess triggers capable of inducing the necessary conformational changes that facilitate viral membrane fusion or penetration (Inoue et al. 2011). Examples of cellular triggers include receptors, low pH, proteases, chaperones, and reductases. Additionally, because viral replication and assembly often occur in the context of virus-induced membranous structures derived from host membranes, the membranous network of choice should accommodate these remodeling reactions (Miller and Krijnse-Locker 2008). Moreover, as a virus commonly manipulates the host immune system to sustain infection, a membrane’s ability to provide the virus with such an opportunity would offer tremendous advantages during the infection course (Takeuchi and Akira 2009).
A wealth of data implicates the endoplasmic reticulum (ER), one of the most elaborate membranous networks in a cell (Shibata et al. 2009), as the organelle many viruses exploit during infection. This review focuses on how viruses co-opt the ER to enter, replicate, and assemble in the target cell. We will also draw parallels from the mechanisms by which bacterial toxins use the ER for entry. Together, these insights should unveil clues regarding why many viruses select the ER during infection.
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