2) This study presents a two-strain stochastic model to understand the factors influencing the fitness and evolution of SARS-CoV-2 variants. The model accounts for important factors like asymptomatic transmission, mutations, disease import, and the possibility of spillover events
3) โถ๏ธ Variants with milder symptoms may spread faster than severe variants, as milder cases are less likely to seek medical care and get isolated early on. However, this can still result in high hospitalizations and fatalities due to widespread infection.
4) โถ๏ธ Increased transmissibility of milder variants is a concern, as they can infect a larger segment of the population compared to more severe variants.
โถ๏ธ Prolonged infectiousness of variants, even by just a day, can significantly enhance their fitness and ...
5) ...lead to their dominance over previous strains.
โถ๏ธ The global sensitivity analysis reveals that transmission rates and recovery rates are key drivers of variant dynamics, with complex interactions between parameters influencing the wild-type strain.
6) The model provides a nuanced view of viral evolution and transmission dynamics, highlighting the need for robust surveillance, vaccination, and tailored public health interventions to manage the spread of SARS-CoV-2 variants effectively.
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IS SARS-CoV-2 BECOMING "INVISIBLE"? The Hidden Truth Behind the Pandemic
As the world strives to move past the COVID-19 pandemic, a troubling narrative has emerged: the perception that SARS-CoV-2 is becoming "invisible."
2) Governments and communities are eager to return to normalcy, leading to a tendency to downplay the virus's severity. Reports of new infections and long COVID cases have been totally minimized, creating a false sense of security ...
3) ...that the virus is no longer a significant threat. However, this perception is not only a matter of public sentiment. The virus itself has evolved, most notably with the emergence of the Omicron variant. Recent research reveals that Omicron exhibits a remarkable ability ...
2) This research shows that SARS-CoV-2, the virus that causes COVID-19, stops infected cells from dying. Normally, when cells die, it helps stop viruses from spreading. By keeping these cells alive longer, SARS-CoV-2 allows itself to multiply and also helps other viruses ...
3) ... like influenza A, grow more easily.
When someone has both SARS-CoV-2 and influenza A, the two viruses can make a person much sicker. The immune system gets overwhelmed, leading to more inflammation and damage to the lungs.
ENTROPY UNLEASHED:
How Viral Protein Interactions Drive Coronavirus Adaptation in Bats and Humans
Entropy, in a general sense, refers to the level of disorder or randomness in a system. biorxiv.org/content/10.110โฆ
2) When we talk about protein interactions and viral behavior, entropy can be viewed as a measure of how complex and varied these interactions are.
In the context of the study about coronavirus interactions in bat and human cells, here's a simplified breakdown.
3) **Complex Interactions**: The study identifies how proteins from the coronavirus interact with host cells (both bats and humans). These interactions can be highly ordered (low entropy) or more chaotic (high entropy).
Patients care most about how COVID-19 affects their health and daily life, including for those with long COVID. Scientists focus on understanding the virus to find better treatments. Both views are important for dealing with the pandemic.
2) I'm bringing up this topic because, after talking so much about the disease, its long-term effects, treatments, and vaccines, many people have forgotten that we are dealing with the most dangerous virus humanity has ever faced.
Organelles provide the possibility for the virus to organize its RNA in PROTECTED structures, concentrate REPLICATION machinery ... nature.com/articles/s4146โฆ
2) ...compartmentalize the replication process, and hide from immune detection.
Figure 1g - The large perinuclear clusters of viral RNA demonstrate how the viral RNA is organized into PROTECTED structures.
2) Figure 3d- The nanoscale puncta of the viral RNA-dependent RNA polymerase (nsp12) within and around the viral RNA clusters show the concentration of REPLICATION machinery.