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الانزيمات
Adenovirus Coinfection with SARS-CoV-2
المؤلف:
Dhurgham Hassan Shatti Al-Fatlawi
المصدر:
Gene Polymorphisms and Levels of some Immunological Markers in Patients with COVID-19 Pneumonia Associated with Adenovirus as Coinfection - اطروحة دكتوراه - جامعة كربلاء
الجزء والصفحة:
p39-42
2025-03-13
62
In 1953, Human adenoviruses (HAdV) were identified, a cytopathogenic agent was discovered during the long-term cultivation of tonsil and adenoid tissues following procedures on children (Huebner et al., 1954). This established the viruses' names (adenoid degeneration viruses) and provided a basic description of their ecology in relation to asymptomatic persistence in the lymphoid tissue. Adenoviruses were quickly discovered in samples taken from individuals who had conjunctivitis and acute respiratory illnesses (Robbins et al., 1950).
The adenovirus the genome consists of five primary transcriptional units, notably E1A, E1B, E2, E3, as well as E4, which are sequentially present during the viral replication cycle. Genes that encode proteins are found in these transcription units and process of replication of the viral genome entails the participation of several components, and it is has five later transcription units. Proteins that are involved in capsid construction or are part of the viral capsid are encoded by the letters L1 through L5. The L1-L5 later transcription units are all controlled by the same promoter region and share the same transcription start point (Stasiak and Stehle,2020).
Adenoviruses are resistant to environmental stressors and stable to physical or chemical agents as well as pH conditions, allowing them to survive outside of the body for lengthy periods of time. Adenoviruses can be transmission of the virus occurs by the dissemination of respiratory droplets between individuals, as well as through fecal-oral pathways. The cellular receptors for coxsackievirus and Adenoviruses, the first step in the Penetrate of human adenoviruses is adhesion of a virus particle to a target cell by adhesion receptor is the adenovirus receptor, which facilities the internalization of adenoviruses (Bansal et al., 2003). CAR interacts with a particular location just on fiber knob domain. Importantly, constraints need that the Human Adenoviruses fibers be wide and flexible in order to allow receptor binding (Wu E et al., 2003).
It has been established that Human Adenoviruses species serotype A, C, D, E, and F require CAR for adherence, by contrast, Human Adenoviruses species B has the shortest fibers and relies mostly on fiber binding to CD46 or, less commonly, on desmoglein2. Other receptors, such as sialic acid-containing polysaccharides, GD1a glycan, and SR-A6 receptor, have been demonstrated to induce Human Adenoviruses internalization in a range of different cell lines for various Human Adenoviruses types (Baker et al., 2019).
CAR helps to create tight junctions and adherens junctions between epithelial cells (Walters et al., 2002). The receptor with a high specificity contact, however, is cannot ability stimulate viral entrance inside cells. In contrast, the process of catching the virus is accelerated by a subsequent interaction that occurs between the penton base protein of the virus as well as v3 or v5 integrins (Wickham et al., 1993).
Mention a previous report that revealed viral titers in human blood as well as other tissue samples, in addition to serologic and histopathological evidence for infected (Tollefson et al., 2017). Human adenoviruses are frequently encountered as a causative agent of infectious. Adenovirus-associated epidemic conditions were reported extensively in the beginning part of the 20th century. It is worth noting that adenoviral infections can give rise to a diverse array of illnesses. Adenoviral strains account for around between two and five percent of pneumonia overall and are projected to contribute to 2-35% of pulmonary illnesses caused by viruses specifically in kids. These viruses are frequently obtained through conjunctiva, throat, as well as fecal samples, with can be spread by pulmonary and fecal-oral routes (Cherry et al., 2014).
Coinfection of Novel coronavirus, along with various other viral infections of the respiratory tract, potentially exerts a substantial influence on the current outbreak of COVID-19. The best course treatment that complicated by co-infection with viral infections, which also makes diagnosis more difficult. Additionally, it can alter clinical symptoms and heighten illness severity, both of which can raise mortality. According to research, 3-21% of COVID-19 patients had additional viral respiratory pathogen infections (Wang et al., 2020b). Human adenoviruses are capable of causing pneumonia acquired in the community, are linked to about 5-7% of these coinfections (Kim et al., 2020a).
Novel coronavirus with Adenovirus coinfection eventually led to acute respiratory of distress syndrome. ICU admission necessary, and clinical enhancement happened with the injection of hydroxychloroquine. in accordance with regional recommendations, there was uncertainty regarding the precise time of the coinfection, and the individual's comorbidities worsened due to an additional risk factor for the development of a severe disease. (Guan et al., 2020).
The precise pathophysiological processes behind the coinfection with SARS-CoV 2 remain unclear. Some possibilities exist Regarding the relatively low prevalence of the virus that causes SARS-CoV-2 in the absence of a predisposing higher risk factor (Xing et al., 2020). In descriptive investigations, a higher proportion of patients with coinfection developed ARDS and septic shock, necessitating ICU admission (Lai et al., 2020).
Human Adenoviruses may remain in susceptible cells in a latency state for a very long time after the lytic infection (Lion, 2014). Adenoids, tonsils, and Peyer's patches are just a few examples of lymphoid tissues where Human Adenoviruses typically persist during latent infection, Once again creating disease symptoms, these latent virus particles have the potential to reactivate, re-infect, and multiply in epithelial cells (Lynch et al., 2011).
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