The "devil's pact" between the VIRUS and the ASYMPTOMATICS !
In an exciting study, researchers have shown, how human behavior can change the evolution of the virus.
2) When the virus evolved from the Wuhan strain to the Delta, due to the measures to limit its transmission, the virus adapted and evolved, by multiplying by 5 the maximum viral load and by 1.5 in the nb of days before the viral load peaks.
3) When Omicron appeared, researchers discovered that BA.1 showed an earlier peak time and shorter viral shedding compared with the pre-Alpha and Alpha variants (Fig. 4b, c).
4) The reduction of the incubation period, from 6.65 days for the pre-Alpha, 5.00 days for the Alpha, 4.50 days for the Beta, 4.41 days for the Delta, and 3.42 days for the Omicron variants, generated more asymptomatics.
5) From the perspective of virus evolution, which maximizes the basic/effective reproduction number, the evolution of a higher proportion of asymptomatic infection is always favored, because transmissions are not limited, when those infected individuals are not isolated.
6) More asymptomatics, and therefore even fewer measures to limit the spread of the virus, which could thus spread almost "invisibly", in as many hosts as possible.
A pact with this evil virus, where the losers are humans.
@DavidJoffe @RadCentrism @UseBy2022 @RealCheckMarker @RolandBakerIII @arijitchakrav @white_bite @AltenbergLee @xabitron1 @triangle24 @gianlucac1 @siamosolocani @crwequine @kasza_leslie @outbreakupdates @NjbBari3 @MeetJess @LauraMiers JN.1 WAVES with HIGH VIRAL PEAKS in wastewater data
(Part 2)
@DavidJoffe @RadCentrism @UseBy2022 @RealCheckMarker @RolandBakerIII @arijitchakrav @white_bite @AltenbergLee @xabitron1 @triangle24 @gianlucac1 @siamosolocani @crwequine @kasza_leslie @outbreakupdates @NjbBari3 @MeetJess @LauraMiers 8) In previous tweets we explained that the characteristics of Omicrons were:
- a viral load which arrives earlier and lasts less time
- an increase in asymptomatics
Virus transmission occurs from an infected individual to susceptible individuals
@DavidJoffe @RadCentrism @UseBy2022 @RealCheckMarker @RolandBakerIII @arijitchakrav @white_bite @AltenbergLee @xabitron1 @triangle24 @gianlucac1 @siamosolocani @crwequine @kasza_leslie @outbreakupdates @NjbBari3 @MeetJess @LauraMiers 9) ...depending on the infected individual’s infectivity, which depends on their viral load.
Why, if the viral load is lower per individual, are we seeing such viral peaks? To understand this, we need to go back to the transmission potential RTP
@DavidJoffe @RadCentrism @UseBy2022 @RealCheckMarker @RolandBakerIII @arijitchakrav @white_bite @AltenbergLee @xabitron1 @triangle24 @gianlucac1 @siamosolocani @crwequine @kasza_leslie @outbreakupdates @NjbBari3 @MeetJess @LauraMiers 10) ...which is calculated from the sum of newly infected individuals [number of contacted individuals per day] × [transmission probability per contacted individual]).
The paradox is that the more asymptomatic people you have (who contaminate without knowing it),
@DavidJoffe @RadCentrism @UseBy2022 @RealCheckMarker @RolandBakerIII @arijitchakrav @white_bite @AltenbergLee @xabitron1 @triangle24 @gianlucac1 @siamosolocani @crwequine @kasza_leslie @outbreakupdates @NjbBari3 @MeetJess @LauraMiers 11) ... the faster the transmission, especially if the peak occurs earlier.
And this, even if the viral peak per individual is lower than in the pre-alpha variants.
JN.1 characterizes an evolution of a “stealth” phenotype showing a decreased peak viral load per individual
@DavidJoffe @RadCentrism @UseBy2022 @RealCheckMarker @RolandBakerIII @arijitchakrav @white_bite @AltenbergLee @xabitron1 @triangle24 @gianlucac1 @siamosolocani @crwequine @kasza_leslie @outbreakupdates @NjbBari3 @MeetJess @LauraMiers 12) ...with a high proportion of asymptomatic infection.
We are therefore witnessing a decoupling between the evolution of virus phenotype and the evolution of clinical phenotype.
Thanks for reading 🙏
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AVIAN FLU for KIDS
What Happens When Viruses Team Up?
Let’s talk about two interesting friends in the virus world: H5N1 and H3N8. They are both types of avian influenza viruses, which means they can make birds sick.
2) Now, what do those numbers mean?
The "H" and "N" in H5N1 and H3N8 are like special codes that tell us something important about each virus. The "H" stands for hemagglutinin, and the number after it (like 5 or 3) tells us which type it is.
3) The "N" stands for neuraminidase, and the number after it (like 1 or 8) tells us its type, too. So, H5N1 has a type 5 "H" and a type 1 "N," while H3N8 has a type 3 "H" and a type 8 "N."
Sometimes these viruses can work together in a really interesting way called reassortment.
IMAGINE You're a SNEAKY SARS-CoV-2 VIRUS :
How You’d Use Blood Vessels to ATTACK the HUMAN BRAIN, Create Chaos, and Confuse the Brain’s Cleanup Crew!
An Informative EXPLANATION based on 3 recent studies, FOR KIDS and EVERYONE !
2) Imagine Our Body as a Big City:
In this city, blood vessels act like roads, allowing cars (our blood cells) to travel everywhere. Sometimes, bad guys called viruses, like SARS-CoV-2, sneak into this city.
2) ▶️ Getting In:
Think of the SARS-CoV-2 virus as a clever thief. It uses the roads (blood vessels) to reach important areas, like the brain. It carries special keys called spike proteins that help it unlock doors in the blood vessel walls to enter.
H5N1 ALARMING ADAPTATIONS:
How Mutations in the Bird Flu Virus are Enabling Spread Between Animals and Posing Grave Pandemic Threat to Humans
(Thanks to @greg_folkers for this new study in Nature) nature.com/articles/s4146…
2) The H5N1 bird flu virus spread quickly along the coast of Chile, infecting wild birds, farm chickens, and sea animals like seals and dolphins.
The virus came from Peru and then moved south through Chile. Importantly, the virus changed in a way that helps it infect and ...
3) ... spread between mammals, including humans.
Specifically, the virus developed mutations in a gene called PB2. These PB2 mutations allow the virus to replicate better and cause more severe illness in mammals.
Unlocking the GENETIC SECRETS BEHIND SEVERE COVID-19 and LONG COVID
An allele is a different version of a gene. Genes are the instructions in our cells that tell our body how to work. But sometimes there are small differences ... medrxiv.org/content/10.110…
2) ...in these instructions, and those different versions are called alleles.
This study found that a gene called MTHFR affects how sick people get from COVID-19.
Fig.1. Plasma metabolomics of COVID-19 patients reveals one-carbon metabolism association with COVID-19 severity
3) MTHFR has different versions, called alleles.
People with a certain MTHFR allele had higher levels of chemicals related to how cells use one-carbon.
Fig. 2. Relative changes in methionine metabolism are correlated with COVID-19 severity
Exploring the Persistence of the Spike Protein along the Skull-Meninges-Brain Axis and the Neurological Effects of COVID-19
This analysis is supported by numerous videos and illustrations.
First, let's identify the location of the skull-meninges-brain axis. Here it is 👇
2) Here is where Spike protein persists in skull marrow, meninges, and brain, accumulating in the recently discovered skull-meninges connections 👇
3) Here are the confoncal images showing SARS-CoV-2 spike and nucleocapsid proteins in skull marrow and meninges of COVID-19 patients, indicating viral presence in these brain border regions.
2) The links between HIV and SARS-CoV-2 highlighted in this study are:
▶️ People living with HIV often have altered T cell responses compared to those without HIV, including lower T cell counts, decreased T cell receptor diversity, and functional changes in CD8+ T cells.
3)▶️ This study found that people living with HIV on antiretroviral therapy still mounted robust T cell responses to conserved regions of the SARS-CoV-2 virus, even if they had not been previously infected with COVID-19.