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Morphology, Pathogenesis, Genome Organization, and Replication of Coronavirus (COVID-19)
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Sadia Javed, Bahzad Ahmad Farhan, Maria Shabbir, Areeba Tahseen, Hanadi Talal Ahmedah, Marius Moga
However, in the clinical findings of COVID-19, three forms of individual reaction to COVID-19 occur. The first form involves individuals who respond ineffectively to an infection and that are unable to control the virus. This results in an exhilarating inflammatory reaction in some individuals. Consequently, virus replication occurs. The second form consists of people who, following infection with immune responses, are asymptomatic or minimally symptomatic and controls the virus successfully without causing undue host damage to disrupt homeostasis. In the third form, those individuals include that either initially respond to damage to COVID-19 tissue or are increasingly inflamed in the lungs by unregulated viral replication [115].
The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Viruses have no intrinsic means to generate energy so they must rely totally on the metabolic machinery of host cells to synthesize new viral components. During viral replication, the nucleic acid of the virus which composes its genome becomes active within the infected cell and serves as a template to make copies of itself and to produce new viral proteins. These newly synthesized proteins and genomic elements assemble into new infectious virions that are released by cell lysis or by budding from the host cell. In some cases the viral genome may incorporate into the host cell DNA leading to persistent infections that may lead to many changes in the host cell including cancer. The genetic information in the virus genome and in the host cell determines the outcome of the virus-cell interaction.
Conventional Pharmacological Strategies, Investigational Drugs, and Immunotherapies for COVID–19
Published in Srijan Goswami, Chiranjeeb Dey, COVID-19 and SARS-CoV-2, 2022
Subhra Bhattacharya, Srijan Goswami, Chiranjeeb Dey
Interferons are immunomodulatory chemicals (cytokines) that may be used as a non-specific antiviral agent. Interferon-α and interferon-β are major pharmacological candidates among others that have shown significant response in the management of COVID-19 patients and are still under clinical trials. The binding of interferon-α and interferon-β to their specific receptors (INF-αR and INF-βR, respectively) leads to the phosphorylation of several transcription factors including STAT-1. The phosphorylated STAT-1 gets translocated into the nucleus where it associates with interferon-stimulated genes (ISGs). This association leads to immunomodulatory and antiviral effects and thus interferes with the viral replication process. Due to a lack of convincing data, the use of interferons for the treatment of COVID-19 patients is not recommended at present (Zhou, 2020; Interferons, 2020; Alavi Darazam et al., 2021).
Effect on SARS-CoV-2 viral load using combination therapy with casirivimab/imdevimab and remdesivir
Published in Baylor University Medical Center Proceedings, 2022
Vivek K. Kataria, Mezgebe Berhe, Uriel Sandkovsky
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in an ongoing pandemic, in which disease severity and spectrum vary significantly. Established risk factors for severe disease consist of vaccination status, underlying comorbidities, and age ≥65 years.1–4 Moreover, recent evidence suggests that high SARS-CoV-2 viral load is an independent predictor of disease severity and mortality.5 While management largely consists of supportive care, numerous therapeutics have been developed to augment viral replication and/or host immune response to mitigate disease progression and improve clinical outcomes. Current pharmacologic treatment strategies for patients with SAR-CoV-2 consist of monoclonal antibody therapy, antiviral medications, and anti-inflammatory agents. While anti-inflammatory agents and the antiviral remdesivir are almost exclusively utilized in severe disease, monoclonal antibodies are commonly utilized in patients with nonsevere disease who have a high risk for progression. Phase 3 clinical trials are limited to nonhospitalized patients with mild to moderate COVID-19; however, ongoing studies have investigated the role of monoclonal antibodies in hospitalized patients.6–9 We report a case of severe COVID-19 treated with casirivimab/imdevimab and remdesivir, in which quantitative nasopharyngeal (NP) viral loads were trended throughout the hospital/treatment course.
The roles of epidermal growth factor receptor in viral infections
Published in Growth Factors, 2022
Progeny virions may spread to the adjacent cells via extracellular or intracellular route and cause localised infection. In extracellular spread, virions are dispersed into the extracellular fluid and infect neighbouring cells. While some viruses infect adjacent cells intracellularly via the fusion between infected cells and uninfected cells or by cytoplasmic bridges formed between cells. Alternatively, virus may disseminate throughout the body and cause systemic infection via lymphatic and haematogenous routes or through infected migratory cells like lymphocytes and macrophages (Baron, Fons, and Albrecht 1996; Burrell, Howard, and Murphy 2017). Viruses like herpesvirus and rabies virus are able to disseminate through nerves and invade the central nervous system. On the other hand, some viruses are able to establish latent infection by lying dormant in the infected cells. In response to several stress factors, they are reactivated to lytic stage and cause productive viral replication and spread (Traylen et al. 2011). Recent studies have revealed viruses exploit the function of EGFR to promote viral replication, spread and establishment of latency (Table 2).
Immunobiology and nanotherapeutics of severe acute respiratory syndrome 2 (SARS-CoV-2): a current update
Published in Infectious Diseases, 2021
Ifeanyi Elibe Mba, Hyelnaya Cletus Sharndama, Goodness Ogechi Osondu-chuka, Onyekachi Philomena Okeke
Generally, several factors affect the production of novel antiviral drugs. The rapid increase in drug resistance is one of the significant factors. Moreover, the multiplication of viruses using host cell machinery makes it difficult to target specific viral metabolic pathways without impacting the host cell. Also, the fact that each virus has a unique biosynthetic pathway makes the formulation of drugs targeting a wide range of viruses highly difficult. Viral replication is dependent on the biosynthetic machinery of the host cell [202]. Thus, only a limited number of virus-specific metabolic functions that antiviral drugs can target without any damage to the host cells. Also, each virus has a specific role. This attribute hinders the formulation of a broad-spectrum antiviral agent that causes similar symptoms. Even some drugs that can cure acute illness are not effective during latent infection. This can lead to recurrent or chronic disease, which always poses some treatment difficulties [201]. Thus, drug preparation or dosage manipulation that targets physicochemical and bio-pharmaceutical features of antiviral materials should be a new therapeutic tactic.