2) This study examined how co-infection with SARS-CoV-2 and dengue virus can impact the evolution of SARS-CoV-2 variants.
The key findings are:
- 2% of COVID-19 patients in the study area also had dengue virus infection. These co-infected patients showed more severe symptoms ..
3) ...like headaches and loss of smell/taste.
- Genetic analysis revealed the co-infected patients had significantly more mutations in the SARS-CoV-2 virus compared to those with COVID-19 alone.
4) - Mathematical modeling estimated that the emergence of the Delta variant required about 9-12 more mutations than earlier variants, while the Omicron variant accumulated about 19 more mutations than Delta.
5) - The increased mutations in co-infected cases suggest the compromised immune system allows the virus to adapt and evolve more easily. This could lead to the emergence of new SARS-CoV-2 variants, especially when dengue and COVID-19 are circulating together.
6) - Ongoing monitoring of viral mutations and studying co-infection effects are important to anticipate and prepare for potential future SARS-CoV-2 variant outbreaks.
There are some limitations in this study as the potential underestimation of coinfection prevalence,
7) ...the small coinfection sample size and the limited clinical data.
Thanks for reading π
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What is the BUTYRATE-PRODUCING BACTERIA?
A bacteria of the naso-oropharyngeal microbiome which may have a protective role against severe COVID-19 disease ?
- Bacteria belonging to the butyrate-producing phyla Bacillota and Bacteroidota were more abundant in SARS-CoV-2 infected individuals before vaccines were available.
3)- Butyrate, the compound produced by these bacteria, has known beneficial effects like reducing inflammation and strengthening protective barriers in the body.
3. The relatively low severity of COVID-19 observed in the African population studied was hypothesized ...
MEMBRANE FUSION is a CRUCIAL STEP in the INFECTION process of CELLS by SARS-CoV-2
(last partπ§΅)
Membrane fusion of JN.1-derived SARS-CoV-2 SLip, FLiRT, and KP.2 variants
2) We will examine this study we've previously posted solely from the perspective of membrane fusion. The graphics may not directly align with the text.
This study provides the following key details about membrane fusion for the JN.1-derived Omicron subvariants.
3) - Cell-cell fusion assays were used to measure the fusogenicity of the different spike proteins.
- Compared to the ancestral D614G variant, the JN.1 parental strain exhibited markedly reduced cell-cell fusion activity in both 293T-ACE2 and CaLu-3 cell lines.
2) This study shows that the spike protein needs to interact with a specific lipid called phosphatidylserine (PS) on the cell membrane to trigger the fusion process.
3) Using advanced imaging techniques, the researchers found that the spike's fusion peptide directly binds to PS lipids. This binding is enhanced by low pH and calcium ions, which cause the spike to change shape and fuse the viral and cell membranes.
If YOU WERE a VIRUS, would you PRIORITIZE REPLICATING EXTENSIVELY WITHIN a SINGLE HOST (within-host replication) or, FOCUS on SPREADING to the MAXIMUM number of INDIVIDUALS (between-host transmissibility) ?
βΆοΈ ANSWER(S) in this long threadπ§΅
2) To explore various concepts on this topic and address the question, we referred to three studies :
4) The second study is a key reference whose some graphs we will use for illustration,
"Determinants of SARS-CoV-2 within-host evolutionary rates in persistently infected individuals"
2) The study looks at how the levels of the virus (viral load) change over time in people infected with the SARS-CoV-2 virus, specifically the Alpha and Omicron variants.
To measure viral load, the researchers used a test called a PCR test, which gives a "Ct value".
3) The Ct value tells you how much virus is present - the lower the Ct value, the more virus there is.
The researchers developed a model to track how the Ct values, and therefore the viral load, changes as people go from being infected but not showing symptoms (presymptomatic)..
The virus SARS-COV-2, SAYS "THANK YOU" to its HOSTS, the HUMANS
... for providing a key epigenetic regulator, that the virus has learned to imitate for its own advantage π€
(Weekend thread)
Let me explain this incredible mechanism ...π€«
2) The SARS-CoV-2 virus has found a clever way to copy a important part of the human cell. This important part is called histones, which are proteins that help control how the cell's genes are used.
3) By copying or imitating these histones, the virus is able to disrupt the normal controls the human cell has over its genes. This allows the virus to take over the cell and use it to make more copies of itself.