What is the DURATION of IMMUNITY? What is the IDEAL INTERVAL between TWO VACCINATIONS?
Immunity varying among individuals and vaccine effectiveness changing depending on variants, a vaccination strategy can only recommend a sufficiently wide interval. journals.plos.org/plosone/articl…
2) The study presents a comprehensive model to understand disease outbreaks and vaccination strategies. The model considers factors like comorbidity and multiple vaccine doses to analyze epidemic dynamics.
3) The key findings:
- The gap between vaccine doses is crucial - it can significantly impact disease spread. Frequent vaccination may not always be necessary and can reduce immunity over time.
4)- Determining the optimal dosing interval is critical. It should balance factors like immunity levels, vaccine efficacy, and emerging virus variants to effectively manage the disease.
5) - The presence of multiple circulating strains can affect the frequency and severity of epidemic peaks. Optimizing the dose interval can build lasting immunity, reducing the need for frequent vaccination.
6)- An optimal control strategy is proposed to minimize both infections and vaccination costs by finding the right gap between doses based on population immunity.
7) The model provides a versatile framework that can be adapted for different diseases. It challenges the common assumption that frequent vaccination is always better, emphasizing the need for a more nuanced, cost-effective approach to disease control.
8) The study acknowledges limitations like homogeneous population assumption, equal vaccine effectivness and lack of granular data.
In summary, the optimal time between two vaccine doses is not a one-size-fits-all solution, but rather ...
9) ...should be determined by carefully analyzing the population immunity, vaccine efficacy, and cost-effectiveness factors. The study suggests a range of 3-8 months as a potentially optimal interval based on the modeling results.
Thanks for reading 🙏
• • •
Missing some Tweet in this thread? You can try to
force a refresh
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 part🧵)
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) ?
▶️ ANSWER(S) in this long thread🧵
2) To explore various concepts on this topic and address the question, we referred to three studies :
The first study is the most recent,
"Phylogenetic signatures reveal multilevel selection and fitness costs in SARS-CoV-2" wellcomeopenresearch.org/articles/9-85/…
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 🤔
(Weekend thread)
Let me explain this incredible mechanism ...🤫
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.