Physiological Events Leading To Successful Enterovirus Infection

As the research revealing physiological events leading to successful enterovirus infection; Enteroviruses are one of the most common human pathogens leading to high number of acute and chronic infections worldwide. But the physiological events leading to successful enterovirus infection are still poorly understood. The extracellular albumin and endosomal ions prime enterovirus particles for uncoating that can be preventing by fatty acid saturation.

This finding the significant new information concerning; the role of Albumin and ions in host cell vesicles that promote genome release and efficient infection. The results may yield targeting for therapeutic development. Especially the molecular factors that help enteroviruses to open up and release its genome in human cells are not well understood.

The enterovirus infection

But using real-time uncoating measurements; and high-resolution structures. This finding that the common molecule in serum and interstitial fluids, albumin; and an ion composition that is typically developing in cellular vesicles, trigger expansion of the virion. This expanding and fenestrated virus then allowing more small molecules such as ions to enter the virus. The results of this study suggest that before entering cells, albumin primes the virus to form a metastable yet infectious intermediate particle.

Then, ionic changes that are likely to occur in cellular vesicles; further contribute to opening and promote release of the genome. This conversion was blocking by saturating the albumin with fatty acids. High potassium but low sodium and calcium concentrations, mimicking the endosomal environment; also inducing the formation of a metastable uncoating intermediate of echovirus.

Release of the genome

The successful release of the genome is one of the rate-limiting steps in virus infection. It needs to occur in the right place in the right time to ensure efficient infection. This work provides new insight into understanding this fundamental aspect of enterovirus life cycle and may yield targets for therapeutic development. Together, these factors boosted the formation of the uncoating intermediate; and the infectivity of this intermediate was retained, as judged by end-point titration.

The research Extracellular Albumin and Endosomal Ions Prime Enterovirus Particles for Uncoating That Can Be Prevented by Fatty Acid Saturation. The results presented here suggest that extracellular albumin; partially saturated with fatty acids, likely leads to the formation of the infectious uncoating; intermediate prior to the engagement with the cellular receptor. In addition, changes in mono- and divalent cations, likely occurring in endosomes, promote capsid opening and genome release.