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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).
COVID-19 pathogenesis and host immune response
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Surbhi Bihani, Shalini Aggarwal, Arup Acharjee
SARS-CoV-2 and severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) are placed under the Betacoronavirus genus of the Coronaviridae family. The members of Coronaviridae are enveloped with positive-sense, single-stranded RNA viruses (Gorbalenya et al. 2020). Deep sequencing methods have identified that the full-length genomic RNA of SARS-CoV-2 is around ~30 kb long and comprises 14 open reading frames (Kumar 2020). The spike protein enables cellular entry of the virus by interacting with the host cell surface receptor, angiotensin-converting enzyme 2 (ACE2) (Wang et al. 2020). After the receptor-binding domain (RBD) of spike protein comes in close contact with host ACE2, it is subjected to proteolytic priming by a transmembrane serine protease—TMPRSS2—of the host, which is to enable efficient viral–host membrane fusion reaction (Hoffmann et al. 2020). Alternatively, receptor-mediated endocytosis of the viral particle followed by proteolytic priming of S protein by endosomal cathepsin L is another way of viral entry into the host cell (Hoffmann et al. 2020). Once the viral genome is released inside the host cell, ORF1a and ORF1ab are translated into polyproteins and are cleaved into nsps by host and viral proteases (nsp3 and nsp5 harbor papain-like and 3C-like protease domains, respectively) (Harrison, Lin, and Wang 2020). Nsp12 possesses the main RNA-dependent RNA polymerase activity and, with other nsps, forms the Replicase to enable replication of genomic and subgenomic RNAs (sgRNA) (Harrison, Lin, and Wang 2020). Structural and accessory proteins enable the assembly and egress of progeny virions and aid in viral replication and pathogenesis (Yoshimoto 2020). The viral entry and life cycle are summarized in Figure 7.1.
Coldzyme® Mouth Spray reduces duration of upper respiratory tract infection symptoms in endurance athletes under free living conditions
Published in European Journal of Sport Science, 2021
Glen Davison, Eleanor Perkins, Arwel W. Jones, Gabriella M. Swart, Alex R. Jenkins, Hayley Robinson, Kimberly Dargan
Strategies to minimise the risk of contracting a URTI and/or reduce time taken to clear an infection have focussed on avoidance of exposure and minimising the controllable risk factors that are associated with lowered immune defence (e.g. intensified training, life stressors), but these may be difficult to avoid for many athletes (Svendsen et al., 2016; Walsh, Gleeson, & Pyne, 2011). Other strategies have focussed on nutritional interventions purported to reduce the immune perturbations caused by strenuous exercise and training. Unfortunately, many such strategies have limited success (Davison, Kehaya, & Jones, 2016; Keaney et al., 2019; Walsh, 2018; Walsh, Gleeson, & Pyne, 2011; Williams et al., 2019). An alternative strategy that has received little attention in athletic populations, is the use of products that may inhibit viral infectivity (for example, via limiting viral entry or replication/propagation after initial exposure). Most URTIs are caused by viral infection, with over 200 known viruses, the most common being rhinoviruses, coronaviruses, influenza viruses, adenoviruses, parainfluenza viruses, respiratory syncytial viruses and enteroviruses (Heikkinen & Järvinen, 2003). Infection is initially established in the mucosa of the nasopharynx before spreading anteriorly, through the nasal region (Winther, Gwaltney, Mygind, Turner, & Hendley, 1986), with local symptoms typically beginning in the throat before nasal congestion, rhinorrhoea, sneezing and cough tend to develop (Witek, Ramsey, Carr, & Riker, 2015).
COVID-19;-The origin, genetics,and management of the infection of mothers and babies
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Hassan Ih El-Sayyad, Yousef Ka Abdalhafid
Seven human CoVs are known to cause mild diseases such as 229E, OC43, NL63 and HKU1, and the pathogenic species SARS-CoV, MERS-CoV, and SARS-CoV-2. Coronaviruses are spherical (125 nm diameter), and enveloped with club-shaped spikes on the surface giving the appearance of a solar corona. Within the helically symmetrical nucleocapsid is large positive sense, single-stranded RNA. Of the four CoV genera (α,β,γ,δ), human CoVs (HCoVs) are classified under α-CoV (HCoV-229E and NL63) and β-CoV (MERS-CoV, SARS-CoV, HCoVOC43, and HCoV-HKU1). SARS-CoV-2 is a β-CoV and shows fairly close relatedness with two bat-derived CoV-like CoVs, bat-SL-CoVZC45 and bat-SL-CoVZXC21. Even so, its genome is similar to that of the typical CoVs. The SARS-CoV and MERS-CoV originated in bats, and the same origin has been suggested for SARS-CoV-2. The possibility of an intermediate host facilitating the emergence of the virus in humans has already been shown with civet cats acting as intermediate hosts for SARS-CoVs, and dromedary camels acting as intermediate hosts for MERS-CoV. Human-to-human transmission is achieved through close contact with respiratory droplets, direct contact with infected individuals, or by contact with contaminated objects and surfaces. The corona viral genome contains four major structural proteins: the spike (S), membrane (M), envelope (E) and the nucleocapsid (N) protein, all of which are encoded within the 3ʹ end of the genome. These proteins have different functions; the S protein mediates attachment of the virus to the host cell surface receptors resulting in fusion and subsequent viral entry. The M protein is the most abundant protein and defines the shape of the viral envelope. The E protein is the smallest of the major structural proteins and participates in viral assembly and budding. The N protein is the only one that binds to the RNA genome and is also involved in viral assembly and budding. Replication of CoVs begins with attachment and entry. Attachment of the virus to the host cell is initiated by interactions between the S protein and its specific receptor. Following receptor binding, the virus enters the host cell cytosol through cleavage of the S protein by a protease enzyme, followed by fusion of the viral and cellular membranes. The next step is the translation of the replicase gene from the virion genomic RNA and then translation and assembly of the viral replicase complexes. Following replication and subgenomic RNA synthesis, encapsidation occurs resulting in the formation of the mature virus. Following assembly, virions are transported to the cell surface in vesicles and released by exocytosis [98].