Ultrastructure of the replication sites of positive-strand RNA viruses

Abstract

Positive strand RNA viruses replicate in the cytoplasm of infected cells and induce intracellular membranous compartments harboring the sites of viral RNA synthesis. These replication factories are supposed to concentrate the components of the replicase and to shield replication intermediates from the host cell innate immune defense. Virus induced membrane alterations are often generated in coordination with host factors and can be grouped into different morphotypes. Recent advances in conventional and electron microscopy have contributed greatly to our understanding of their biogenesis, but still many questions remain how viral proteins capture membranes and subvert host factors for their need. In this review, we will discuss different representatives of positive strand RNA viruses and their ways of hijacking cellular membranes to establish replication complexes. We will further focus on host cell factors that are critically involved in formation of these membranes and how they contribute to viral replication.

Influenza A virus ribonucleoproteins modulate host recycling by competing with Rab11 effectors

“…This observation supports a functional role for the clusters, instead of them being a byproduct of infection, given that the assembly of the SeV genome deviates from that of a segmented genome, but the SeV altered distribution of Rab11 might reflect the need to concentrate other virion components (Stone et al, 2015). Other roles found for vesicular clustering originating during infection with different types of virus include the formation of structures for escaping host anti-viral responses or for recruiting membrane, which is a pre-requisite for the budding of enveloped virions (Harak and Lohmann, 2015;Laliberte and Moss, 2010;Fig. 8.…”

Building Viral Replication Organelles: Close Encounters of the Membrane Types

“…Structure, composition, and formation of replication organelles vary greatly between different groups of viruses and even between viruses belonging to the same family [2,3]. In general, replication organelles can have one of two distinct types of morphology ( Fig 1 ).…”

“…Enteroviruses primarily target the Golgi complex to generate replication organelles, whereas cardioviruses and HCV are proposed to target ER membranes. As a common principle, these viruses all recruit a host PI4P kinase—albeit different isoenzymes—to enrich PI4P at their replication organelles (Fig 1C) [3,14,17]. For example, enteroviruses hijack the Golgi-derived isoenzyme PI4KIIIβ, while cardioviruses and HCV hijack the ER-resident PI4KIIIα.…”

“…Regardless of which isoenzymes these viruses usurp, all PI4Ks are recruited to enrich the respective replication organelles in PI4P lipids. Likewise, in all cases, the PI4P lipids serve to recruit OSBP to the replication organelles, leading to the formation of vMCSs between the ER and the replication organelle at which a cholesterol/PI4P exchange drives the accumulation of cholesterol at replication organelles [3,14,16,18]. …”

Are viruses alive? The replicator paradigm sheds decisive light on an old but misguided question

“…Among other processes, non-producers can contribute to energy conversion as is the case with cyanophages many of which encode cyanobacterial photosystems (Clokie and Mann 2006; Thompson et al 2011). Furthermore, even small non-producing replicators, such as RNA viruses, affect modifications of the host cell metabolism and the formation of structures, such as virus factories, that channel substrates into viral genome replication (Harak and Lohmann 2015; Romero-Brey and Bartenschlager 2014). All the prowess of viruses in the modulation of the host metabolism notwithstanding, producers and non-producers are clearly distinct: to the best of our current knowledge, non-producers never direct the formation of energizable membranes, extremely rarely encode complete metabolic pathways and never a complete translation system (Koonin and Dolja 2013; Raoult and Forterre 2008).…”