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Self-Assembling Protein Nanomaterials – Design, Production and Characterization
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Bhuvana K. Shanbhag, Victoria S. Haritos, Lizhong He
Viruses protect their genetic material by encapsulating them within protein capsids that are composed of protein subunits called capsomeres, which self-assemble in vivo during viral replication. VLPs are formed from capsomeres, themselves produced by recombinant expression, and retain their self-assembling ability under in vitro conditions but lack virus genetic material. As they lack viral genetic material, VLPs are non-pathogenic and the hollow capsids are ideal for encapsulating substances within or displaying desired molecules on the surface. Due to these attributes, VLPs find wide application in the field of vaccine development and drug delivery (Ding et al., 2018). Therefore, the typical design considerations for VLP subunits include interface design for controlled in vitro assembly, improving stability of VLPs, surface modifications for antigen presentation, and mutations to interior and exterior surfaces for functionalisation (Frietze, Peabody and Chackerian, 2016; Hill et al., 2017).
Virus-Based Nanobiotechnology
Published in Yubing Xie, The Nanobiotechnology Handbook, 2012
Magnus Bergkvist, Brian A. Cohen
The viral life cycle can be generalized by three or four phases: (1) viral entry, (2) replication, (3) shedding, and/or (4) latency. Each phase in the viral life cycle consists of a multitude of specific interactions at the nanoscale, making them prime candidates for use as biotemplates or nanoengineering scaffolds, as will be discussed later. Infection begins with viral entry into the host cell. This requires the binding of viral attachment proteins to receptors on the target cell surface, or fusion of the viral envelope to the cell membrane, followed by internalization of the virus’s genetic material, and depending on the virus, replication proteins. During replication, the virus takes control of the host cell’s machinery, directing it to synthesize copies of viral nucleic acids and proteins, which then self-assemble into a functional virion. Phase three consists of the escape of the viral progeny from the host cell. The fourth phase—latency—occurs when under certain circumstances, such as evasion of host cell defense mechanisms, the virus may incorporate its genetic material into that of the host, and wait for more favorable conditions to replicate (Knipe et al. 2007).
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Published in Daniela Colombini, Enrico Occhipinti, ERGOCHECK for a Preliminary Mapping of Risk at Work, 2020
Daniela Colombini, Enrico Occhipinti
Viruses do not have a cellular architecture as they are comprised only of nucleic acid, either DNA or RNA, featuring a variety of different structures (single-stranded or double-stranded, linear or circular) and proteins that coat the genetic material, called capsids. They are generally much smaller than bacteria, their dimensions being in the order of nanometers, and they have a helical or icosahedral structure. Viruses have a protein coating that both protects the nucleic acid from degradation due to the extracellular environment and enables the virus to adhere to specific receptors on the cytoplasmic membrane of the host cell. Viruses have no metabolic functions and are unable to reproduce autonomously; being obligatory intracellular parasites, they grow and can only reproduce in the cells of specific hosts, which may be animals, plants, fungi, etc. Viral replication begins with attachment or adsorption between the virus and the host cell membrane. The virus particle then enters the cell and releases nucleic acid, which begins to express itself. This triggers intense metabolic activity in the cell to enable the expression of the viral genome, its replication and the production of structural proteins that then build new viruses. Ultimately, viral particles are released by the host cell when the cell ruptures or by budding at the outer cytoplasmic membrane. Viral offspring then infect new host cells. Many viruses are harmful to humans, and some are extremely widespread, such as those that cause childhood exanthematous diseases (such as measles, rubella, etc.), influenza and parainfluenza viruses and hepatitis viruses (A, B, C, etc.); others are less known and are localized in specific geographical areas (e.g., Ebola). The diseases that they cause in humans present very different symptoms and may vary in severity from colds and influenza to life-threatening conditions like hepatitis, Acquired Immune Deficiency Syndrome (AIDS), etc.
Preparation and characterization of nanofibrous mats to enhance the anti-viral properties of nonwoven fabrics in medical sectors
Published in The Journal of The Textile Institute, 2023
Dina M. Hamoda, Doaa H. Elgohary, Marwa Abou Taleb
Viruses are not living organisms themselves, but small structures containing only a nucleic acid genome within a mostly protein based protecting membrane. Unlike living organisms, viruses must penetrate a living host cells to reproduce and replicate (Jarach et al., 2020). Although there are variations among different species of viruses, the replication of the virus goes through essential steps: (1) Attachment: the protein of the virus interacts with receptors on the host cell. (2) Penetration: where the viral and cellular membranes fuse. (3) Un-coating: when the virus releases its genes into the cell. (4) Replication: the cell synthesizes viral components, viz., mRNA, proteins, and DNA/RNA, depending on the type of virus. (5) Assembly: where sufficient viral nucleic acids and proteins gather to produce virus particles. (6) Release: budding on of the cell surface discharges virus particles from the host. Each stage in viral replication is a potential target for an antiviral agent. Viruses profoundly affect life on this planet, though they themselves are not alive they exist just beyond the boundary between living and nonliving (Bianculli et al., 2020).
Incorporating viruses into soil ecology: A new dimension to understand biogeochemical cycling
Published in Critical Reviews in Environmental Science and Technology, 2023
Xiaolong Liang, Mark Radosevich, Jennifer M. DeBruyn, Steven W. Wilhelm, Regan McDearis, Jie Zhuang
Viruses are obligate intracellular parasites that utilize host metabolism to replicate. It is of critical importance to examine the relationship between viruses and microbial hosts at both cellular and community levels for better understanding the ecological roles of soil viruses. Viral reproduction is dependent on the metabolic machinery of host cells, and the fate of host cells is directly linked to the mode of viral replication, e.g., lytic or lysogenic (Correa et al., 2021; Howard-Varona et al., 2020). The selection of viral reproduction strategies among temperate viruses has a major role in modulating microbial abundance, composition, diversity, and activity, and is impacted by microbial host fitness, cell abundance and many environmental factors (Brum et al., 2016; Weitz et al., 2019). The replication cycles of viruses and the impacts on microbial hosts are shown in Fig. 3. Obligately lytic viruses and temperate viruses reproducing in the lytic mode exert significant impacts on microbial community composition and diversity via selective viral-induced mortality which is often referred to as top-down control over bacterial community (Bouvier & Del Giorgio, 2007; Braga et al., 2020; Fernández et al., 2018; Liang, Wagner et al., 2020). Thus, at the community level, whether viruses are predominantly reproducing in the lytic or lysogenic mode will determine the nature of the impact of viral infection on host microbial community structure and function (Chen et al., 2021; Chevallereau et al., 2022; Wu et al., 2021). However, to what degree viral lytic or lysogenic infections influence soil microbial community structure and biogeochemistry is not well understood. Efforts to characterize the ecological consequences of viral-caused microbial mortality and microbial metabolic network reprograming are desperately needed for better estimate the impact of soil viruses on microbial community turnover and nutrient cycling.