Viral replication is rapid and robust, but it is far from a chaotic process. Instead, successful production of infectious progeny requires that events occur in the correct place and at the correct time. Rotaviruses (segmented double-stranded RNA viruses of the Reoviridae family) seem to govern their replication through ordered disassembly and assembly of a triple-layered icosahedral capsid. In recent years, high-resolution structural data have provided unprecedented insight into these events. In this Review, we explore the current understanding of rotavirus replication and how it compares to replication of other Reoviridae family members.
"However, because it is not the surface viron protein, VP6 protein elicits only the immunity inhibiting intracellular replication of rotavirus in infected intestinal cells , but does not induce neutralizing antibodies which prevent the rotavirus infection. Rotavirus VP4 (which defines P type) and VP7 (which defines G type) are two independent neutralizing antigens, which constitute the outermost layer capsid of rotavirus . Non-glycosylated VP4 forms the spikes of rotavirus that extended from the viral particle surface, while glycosylated VP7 forms the smooth shell of the virion. "
"Capping by VP3 is incompletely efficient, which results in populations of uncapped and partially capped viral transcripts that activate host innate immune responses through the RNA-sensing PRRs RIG-I and melanoma differentiation-associated protein 5 (MDA5) (Broquet et al., 2011; Sen et al., 2011; Uzri and Greenberg, 2013). Genome replication and virion assembly are coordinated within cytoplasmic inclusions, or viroplasms, that likely serve to conceal dsRNA gene segments from detection by the host PRR machinery (Patton et al., 2006; Trask et al., 2012). Newly synthesized DLPs acquire their outer VP4/VP7 layer by budding through the endoplasmic reticulum, after which progeny virions exit the cell by lysis or exocytosis (Desselberger, 2014). "
[Show abstract][Hide abstract] ABSTRACT: The innate immune response involves a broad array of pathogen sensors that stimulate the production of interferons (IFNs) to induce an antiviral state. Rotavirus, a significant cause of childhood gastroenteritis and a member of the Reoviridae family of segmented, double-stranded RNA viruses, encodes at least two direct antagonists of host innate immunity: NSP1 and VP3. NSP1, a putative E3 ubiquitin ligase, mediates the degradation of cellular factors involved in both IFN induction and downstream signaling. VP3, the viral capping enzyme, utilizes a 2H-phosphodiesterase domain to prevent activation of the cellular oligoadenylate synthase (OAS)/RNase L pathway. Computational, molecular, and biochemical studies have provided key insights into the structural and mechanistic basis of innate immune antagonism by NSP1 and VP3 of group A rotaviruses (RVA). Future studies with non-RVA isolates will be essential to understand how other rotavirus species evade host innate immune responses.
Published by Elsevier Inc.
"Rotavirus studies propose that the double-layered particle (DLP)–VP4–NSP4 complex breaches the ER membrane and penetrates into the ER. The viral capsid protein, VP7, re-envelopes the immature particle (DLP) after removal of the ER membrane and NSP4, and forms the infectious triple-layered particle (Tian et al., 1996; Trask et al., 2012). "
[Show abstract][Hide abstract] ABSTRACT: Endoplasmic reticulum (ER) stress is a general term for representing the pathway by which various stimuli affect ER functions. ER stress induces the evolutionarily conserved signaling pathways, called the unfolded protein response (UPR), which compromises the stimulus and then determines whether the cell survives or dies. In recent years, ongoing research has suggested that these pathways may be linked to the autophagic response, which plays a key role in the cell's response to various stressors. Autophagy performs a self-digestion function, and its activation protects cells against certain pathogens. However, the link between the UPR and autophagy may be more complicated. These two systems may act dependently, or the induction of one system may interfere with the other. Experimental studies have found that different viruses modulate these mechanisms to allow them to escape the host immune response or, worse, to exploit the host's defense to their advantage; thus, this topic is a critical area in antiviral research. In this review, we summarize the current knowledge about how RNA viruses, including influenza virus, poliovirus, coxsackievirus, enterovirus 71, Japanese encephalitis virus, hepatitis C virus, and dengue virus, regulate these processes. We also discuss recent discoveries and how these will produce novel strategies for antiviral treatment.
Frontiers in Microbiology 08/2014; 5:388. DOI:10.3389/fmicb.2014.00388 · 3.99 Impact Factor
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