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1301
Human brain organoids to explore SARS‐CoV‐2‐induced effects on the central nervous system
Philipp Niklas Ostermann; Heiner Schaal;
Reviews in Medical Virology, 24.04.2023
Tilføjet 24.04.2023
Severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2) is the causative agent of coronavirus disease 2019 (COVID‐19). In less than three years, an estimated 600 million infections with SARS‐CoV‐2 occurred worldwide, resulting in a pandemic with tremendous impact especially on economic and health sectors. Initially considered a respiratory disease, COVID‐19, along with its long‐term sequelae (long‐COVID) rather is a systemic disease. Neurological symptoms like dementia or encephalopathy were reported early during the pandemic as concomitants of the acute phase and as characteristics of long‐COVID. An excessive inflammatory immune response is hypothesized to play a major role in this context. However, direct infection of neural cells may also contribute to the neurological aspects of (long)‐COVID‐19. To mainly explore such direct effects of SARS‐CoV‐2 on the central nervous system, human brain organoids provide a useful platform. Infecting these three‐dimensional tissue cultures allows the study of viral neurotropism as well as of virus‐induced effects on single cells or even the complex cellular network within the organoid. In this review, we summarize the experimental studies that used SARS‐CoV‐2‐infected human brain organoids to unravel the complex nature of (long)‐COVID‐19‐related neurological manifestations.
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1302
Inflammatory and vascular biomarkers in post‐COVID‐19 syndrome: A systematic review and meta‐analysis of over 20 biomarkers
Shin Jie Yong; Alice Halim; Michael Halim; Shiliang Liu; Mohammed Aljeldah; Basim R. Al Shammari; Sara Alwarthan; Mashael Alhajri; Abdulsalam Alawfi; Amer Alshengeti; Faryal Khamis; Jameela Alsalman; Abeer N. Alshukairi; Nujoud A. Abukhamis; Fatimah S. Almaghrabi; Souad A. Almuthree; Abdulrahman M. Alsulaiman; Bashayer M. Alshehail; Amal H. Alfaraj; Shorouq A. Alhawaj; Ranjan K. Mohapatra; Ali A. Rabaan;
Reviews in Medical Virology, 24.04.2023
Tilføjet 24.04.2023
Severe acute respiratory syndrome coronavirus 2 may inflict a post‐viral condition known as post‐COVID‐19 syndrome (PCS) or long‐COVID. Studies measuring levels of inflammatory and vascular biomarkers in blood, serum, or plasma of COVID‐19 survivors with PCS versus non‐PCS controls have produced mixed findings. Our review sought to meta‐analyse those studies. A systematic literature search was performed across five databases until 25 June 2022, with an updated search on 1 November 2022. Data analyses were performed with Review Manager and R Studio statistical software. Twenty‐four biomarkers from 23 studies were meta‐analysed. Higher levels of C‐reactive protein (Standardized mean difference (SMD) = 0.20; 95% CI: 0.02–0.39), D‐dimer (SMD = 0.27; 95% CI: 0.09–0.46), lactate dehydrogenase (SMD = 0.30; 95% CI: 0.05–0.54), and leukocytes (SMD = 0.34; 95% CI: 0.02–0.66) were found in COVID‐19 survivors with PCS than in those without PCS. After sensitivity analyses, lymphocytes (SMD = 0.30; 95% CI: 0.12–0.48) and interleukin‐6 (SMD = 0.30; 95% CI: 0.12–0.49) were also significantly higher in PCS than non‐PCS cases. No significant differences were noted in the remaining biomarkers investigated (e.g., ferritin, platelets, troponin, and fibrinogen). Subgroup analyses suggested the biomarker changes were mainly driven by PCS cases diagnosed via manifestation of organ abnormalities rather than symptomatic persistence, as well as PCS cases with duration of
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1303
Sphingosine‐1‐phosphate related signalling pathways manipulating virus replication
Lu Zhang; Juan Liu; Erya Xiao; Qingzhen Han; Lin Wang;
Reviews in Medical Virology, 24.04.2023
Tilføjet 24.04.2023
Viruses can create a unique cellular environment that facilitates replication and transmission. Sphingosine kinases (SphKs) produce sphingosine‐1‐phosphate (S1P), a bioactive sphingolipid molecule that performs both physiological and pathological effects primarily by activating a subgroup of the endothelial differentiation gene family of G‐protein coupled cell surface receptors known as S1P receptors (S1PR1‐5). A growing body of evidence indicates that the SphK/S1P axis is crucial for regulating cellular activities in virus infections like respiratory viruses, enteroviruses, hepatitis viruses, herpes viruses, and arboviruses replicate. Depending on the type of virus, pro‐ or anti‐viral activities of the SphK/S1P axis sometimes rely on the host immune system and sometimes directly through intracellular signalling pathways or cell proliferation. Recent research has shown novel roles of S1P and SphK in viral replication. Sphingosine kinase isoforms (SphK1 and SphK2) levels can be manipulated by several viruses to promote the effects that are expected. Regulation of cellular signalling pathways plays a significant role in the mechanism. The purpose of this review is to provide insight of the characters played by the SphK/S1P axis throughout diverse viral infection processes. We then assess potential therapeutic methods that are based on S1P signalling and metabolism during viral infections.
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1304
Recent developments on Junin virus, a causative agent for Argentine haemorrhagic fever
Sumit Kumar; Dharna Yadav; Divya Singh; Kriti Shakya; Brijesh Rathi; Poonam;
Reviews in Medical Virology, 24.04.2023
Tilføjet 24.04.2023
Junin virus consists of ribonucleic acid as the genome and is responsible for a rapidly changing tendency of the virus. The virus is accountable for ailments in the human body and causes Argentine Haemorrhagic Fever (AHF). The infection is may be transmitted through contact between an infected animal/host and a person, and later between person to person. Prevention of outbreaks of AHF in humans can be a tough practice, as their occurrence is infrequent and unpredictable. In this review, recent information from the past 5 years available on the Junin virus including the risk of its emergence, infectious agents, its pathogenesis in humans, available diagnostic and therapeutic approaches, and disease management has been summarised. Altogether, this article would be highly significant in understanding the mechanistic basis behind virus interaction and other processes during the life cycle. Currently, no specific therapeutic options are available to treat the Junin virus infection. The information covered in this review could be important for finding possible treatment options for Junin virus infections.
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