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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).
Synthesis and Characterization of Nanoparticles as Potential Viral and Antiviral Agents
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
Deepthi Panoth, Sindhu Thalappan Manikkoth, Fabeena Jahan, Kunnambeth Madam Thulasi, Anjali Paravannoor, Baiju Kizhakkekilikoodayil Vijayan
Antiviral nanoparticles are antiviral agents used to control or treat viral infections. The antiviral agents primarily target the different stages of a virus life cycle, and thus, the antiviral drugs perform by inhibiting the viral replication cycle at various stages. Here in this section, we will discuss the synthesis and characterization of different types of antiviral nanoparticles that are utilized as a potential antiviral agent.
Nanoprotection from SARS-COV-2: would nanotechnology help in Personal Protection Equipment (PPE) to control the transmission of COVID-19?
Published in International Journal of Environmental Health Research, 2023
Zhi Xin Phuna, Bibhu Prasad Panda, Naveen Kumar Hawala Shivashekaregowda, Priya Madhavan
The pathogenesis of SARS-Cov-2 is highly associated with its life cycle. The viral life cycle consists of five steps, including attachment, penetration, biosynthesis, maturation, and release (Figure 2). In general, SARS-CoV-2 first binds to angiotensin-converting enzyme 2 (ACE2) and host factors such as type II transmembrane serine protease (TMPRSS2). TheTMPRSS2 will clear ACE2 and activate S proteins to allow viral entry via interaction between SI subunits and receptor binding domain (RBD). This is then followed by viral and host membrane fusion via S2 subunit. Upon entry, the genomic RNA is subjected to immediate translation of two large open reading frames, ORF1a and ORF1b to produce two large overlapping polyproteins pp1a and pp1b. They are then co-translationally and post-translationally processed into individual non-structural proteins (nsps) that are responsible for viral replication and transcription complex. Many of the nsps subsequently form replicase-transcriptase complex (RTC) in double membrane vesicles. The complex transcribes an endogenous genome template of viral entry to negative-sense of both progeny genome and sub-genomic RNA as intermediate products, followed by transcription to positive-sense mRNAs that are mainly mediated by RNA-dependent RNA polymerase (RdRp). Translated structural and accessories proteins (M, S, and E proteins) from sub-genomic proteins are then translocated to endoplasmic reticulum and transited through endoplasmic reticulum-Golgi intermediate compartment (ERGIC). New genomic RNAs are produced upon interacting with structural and accessories protein and N proteins, followed by budding and releasing from infected cells through exocytosis (Astuti and Ysrafil 2020; V’Kovski et al. 2020).