Viral and Host Genetic and Epigenetic Biomarkers Related to SARS-CoV-2 Cell Entry, Infection Rate, and Disease Severity

Gašperšič, Jernej; Dolžan, Vita

doi:10.3390/biology11020178

Cited by 6 publications

(7 citation statements)

References 81 publications

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“…The few virions that establish infection and the low probability of variant transmission during acute infection [2, 12, 13], especially for Omicron with its shorter serial interval [14], still give rise to large clone sizes as observed here. Many of those variants will die out, because those individuals have low contact rates, or host gene variants may reduce cellular entry and viral replication [15], or the variant is less fit. Expansion of some clones is likely due to a combination of super-spreader events and variant fitness [16], an investigation of which would require further epidemiological and genetic analysis.…”

Section: Discussionmentioning

confidence: 99%

SARS-COV-2 Delta and Omicron community transmission networks

Murray

Schvoerer

et al. 2022

Preprint

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To date, calculations of SARS-CoV-2 transmission networks at a population level have not been performed. Networks that estimate infections between individuals and whether this results in a mutation, can evaluate fitness of a mutational clone by how much it expands in number as well as determining the likelihood a transmission results in a new variant. Transmission networks of SARS-CoV-2 infection between individuals in Australia were estimated for Delta and Omicron variants using a novel method. Many of the sequences were identical, with clone sizes following power law distributions driven by negative binomial probability distributions for both the number of infections per individual and the number of mutations per transmission (mean 1.0 nucleotide change for Delta and 0.79 for Omicron). Using these distributions, an agent based model was able to replicate the observed clonal network structure, providing a basis for more detailed COVID-19 modelling. Recombination events, tracked by insertion/deletion (indel) patterns, occurred for each variant in these outbreaks. The residue at position 142 in the S open reading frame (ORF), frequently changed between G and D for Delta sequences, but this was independent of other mutations. On the other hand, several Omicron mutations were significantly connected across different ORF. This model reveals key transmission characteristics of SARS-CoV-2 and may complement traditional contact tracing and other public health strategies. This methodology can also be applied to other diseases as genetic sequencing of viruses becomes more commonplace.

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Section: Discussionmentioning

confidence: 99%

SARS-COV-2 Delta and Omicron community transmission networks

Murray

Schvoerer

et al. 2022

Preprint

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“…Analysis of changes in IFN-λ3 during the course of COVID-19 revealed that patients transitioning from mild to severe disease show a characteristic peak value a few days before the transition (9). The change is (P4) (15). Single nucleotide polymorphisms (SNPs) in ACE2 and TMPRSS2 might contribute to selective binding of SARS-CoV-2.…”

Section: Interferon-lambda 3 (Ifn-λ3)mentioning

confidence: 99%

Tools and factors predictive of the severity of COVID-19

Sugiyama

2023

GHM

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The outbreak of the novel coronavirus infection caused worldwide confusion. The problem with this infection is that it causes severe illness in some patients, resulting in a high rate of death if appropriate treatment is not given. If patients with severe illness that requires treatment are appropriately identified, treatment can be focused on these patients. However, in the early days of the COVID-19 outbreak, the inability to predict and diagnose the disease led to hospitals being overwhelmed. Therefore, various methods for the diagnosis of severe disease were developed early on, and various methods are still being investigated to predict high-risk patients. The currently available prediction methods are divided into those that predict the onset of severe disease and those used to determine the severity of the disease. Specifically, the main methods include genetic factors, serum humoral factors, laboratory tests, and diagnostic imaging. Since each of these factors has different features, using them in combination is likely to be advantageous.

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“…Conversely, viruses can regulate host miRNA to suppress the host im mu ne sy st em . Prev ious s tu dies hav e id en t i fi e d differentially expressed miRNAs in COVID-19 patients through transcriptome analysis (1)(2)(3)(4)(5). In particular, virus RNA can play as sponge of host miRNA to regulate immune processes.…”

Section: Introductionmentioning

confidence: 99%

3’UTR of SARS-CoV-2 spike gene hijack host miR-296 or miR-520h to disturb cell proliferation and cytokine signaling

et al. 2022

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has becoming globally public health threat. Recently studies were focus on SARS-CoV-2 RNA to design vaccine and drugs. It was demonstrated that virus RNA could play as sponge to host noncoding RNAs to regulate cellular processes. Bioinformatic research predicted a series of motif on SARS-CoV-2 genome where are targets of human miRNAs. In this study, we used dual-luciferase reporter assays to validate the interaction between 3’UTR of SARS-CoV-2 S (S-3’UTR) gene and bioinformatic predicted targeting miRNAs. The growth of 293T cells and HUVECs with overexpressed S-3’UTR was determined, while miRNAs and IL6, TNF-α levels were checked in this condition. Then, miR-296 and miR-602 mimic were introduced into 293T cells and HUVECs with overexpressed S-3’UTR, respectively, to reveal the underlying regulation mechanism. In results, we screened 19 miRNAs targeting the S-3’UTR, including miR-296 and miR-602. In 293T cell, S-3’UTR could inhibit 293T cell growth through down-regulation of miR-296. By reducing miR-602, S-3’UTR could induce HUVECs cell proliferation, alter the cell cycle, reduce apoptosis, and enhanced IL6 and TNF-αlevel. In conclusion, SARS-CoV-2 RNA could play as sponge of host miRNA to disturb cell growth and cytokine signaling. It suggests an important clue for designing COVID-19 drug and vaccine.

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Viral and Host Genetic and Epigenetic Biomarkers Related to SARS-CoV-2 Cell Entry, Infection Rate, and Disease Severity

Cited by 6 publications

References 81 publications

SARS-COV-2 Delta and Omicron community transmission networks

SARS-COV-2 Delta and Omicron community transmission networks

Tools and factors predictive of the severity of COVID-19

3’UTR of SARS-CoV-2 spike gene hijack host miR-296 or miR-520h to disturb cell proliferation and cytokine signaling

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