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Dr Nader K. Hijazi Profile picture
@DrNaderKHijazi1
Sep 6, 2020 • 5 tweets • 5 min read • Read on X
@Covid19Crusher @gummibear737 @BallouxFrancois Yes it shows less hospitalized, severe and fatal cases in May-June, and more frequent milder cases. (Look at numbers next to corresponding colors I added) Again pointing to seasonality. It is very clear. What confused many was the continued spread in summer, which is 1/ Image
@Covid19Crusher @gummibear737 @BallouxFrancois Typical in the first wave of a most new pandemic virus (H1N1, Spanish flu) bc most with no immunity. Make no sense to suspect role for Memory Thanks-cells (why show only in the second wave?!), or a sudden mutation. If there are structural / fxnal changes to 🦠 it would be /2
@Covid19Crusher @gummibear737 @BallouxFrancois .. the virus trying to adapt, and in turn become less virulent (it’s trying to survive). Would be interesting to see if some of these mutations are seasonal as well.
Thank you @BallouxFrancois @Covid19Crusher @gummibear737 3/
@Covid19Crusher @gummibear737 @BallouxFrancois * Sorry Memory T-Cells (misspelled by auto filling)
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More from @DrNaderKHijazi1

Dr Nader K. Hijazi Profile picture
May 2, 2022
Some thoughts on the most likely cause of Acute Hepatitis recently seen in children. TLDR: COVID-induced lymphocyte dysfunction leading some pediatric patients to develop severe infection from circulating Adenovirus leading to Acute & Fulminant Hepatitis. 🧵 1/13
1st disclaimer: The exact cause of the recent spike of acute hepatitis cases in children is still unknown, but connecting some dots points to a more likely theory / explanation. Time will tell 2/
The high prevalence of cases with confirmed Adenovirus & COVID in the case series is too high to ignore, and likely much higher than the background general population, making it less likely a coincidence. That was the first clue 3/
Read 13 tweets
Dr Nader K. Hijazi Profile picture
Feb 18, 2022
TIMELY study with Treasure trove of insights on BA.2:

Buries ONCE & FOR ALL that viral evolution is ALWAYS associated with milder diseases:
BA.2 (compared to BA.1):

1.4-fold higher Reproduction number

More replicative & Fusogenic

MORE PATHOGENIC🧵 1/ biorxiv.org/content/10.110…
How many times have we recently heard: SARS-CoV2’s evolutionary path will always make it milder & less pathogenic, giving Omicron as a clear example. Well, we don’t have to wait for another VOC, since a lineage of Omicron BA.2 already proved them WRONG 2/
BA.2 not only is 1.4 times more transmissible, it’s also MORE pathogenic invading more cells in the lower airways (Bronchus, Bronchioles, Alveoli & Lungs 🫁) dependent on TMPRSS2, which is a departure from BA.1. 3/

Read 13 tweets
Dr Nader K. Hijazi Profile picture
Jan 31, 2022
Omicron #BA2 is ~1.5 times more transmissible than original BA1.
Study👇 showing same Viral Load!
Cause will almost certainly be:
Even less Cell Tropism with BA2
More efficient Endosomal entry
➡️ Intrinsically more transmissible,
Not Immune escape 1/ medrxiv.org/content/10.110…
BA.2 will eventually dominate, but thankfully no significant change compared to BA.1 in:
Severity & Clinical picture
Vaccine Efficacy
Response to Antivirals
Reinfection rate

More on why Omicron is more transmissible than other variants here 👇 2/
Scientists are puzzled by the incredibly fast-paced mutations in SARS-CoV2 in general, and Omicron in specific. This trajectory doesn’t bode well for the scenario of Omicron settling into an Endemic profile soon 3/
Read 5 tweets
Dr Nader K. Hijazi Profile picture
Jan 20, 2022
MAJOR recent revelations + Connecting the dots:
1. ⬆️ Omicron infectiousness NOT related to Viral Load
2. Different ‘Cell Entry’ mode
3. ‘With’ or ‘For’ Covid conundrum
4.Delayed deaths > 1 month & ⬆️ Excess death.
Why we should call Omicron: COVID-21. Mega🧵 1/
Omicron is a major shift from other VoC in so many ways we are trying to comprehend.
This🧵 tries to connect separate recent revelations representing more pieces of the Omicron jigsaw puzzle 🧩. It also concludes it’s time to Re-classify Omicron-induced Disease as: COVID-21
2/
Recent studies showed that (despite what we thought) Omicron’s ⬆️ infectiousness is not due to higher Viral Load in the Nasopharynx, like Delta. Another study revealed a Paradigm shift in how Omicron easily enters numerous host cells & replicates faster 3/ medrxiv.org/content/10.110…
Read 28 tweets
Dr Nader K. Hijazi Profile picture
Jan 10, 2022
Some experts are claiming Covid already reached endemicity, like other ‘Seasonal Coronaviruses’, or will in the next few months. Why this is NOT rooted in science or precedent & is just wishful speculation /thinking. We are in uncharted territory. Thread 🧵 1/
How many times have you heard ‘COVID will soon become seasonal & endemic like ALL other Coronaviruses? There are SO many faults in this argument. For 1: Circulating Seasonal Coronaviruses are from a different lineage A (Embicovirus sublineage) 2/ ImageImageImage
Why is this important? They are really different from other known human Sarbecoviruses (MERS-CoV:Lineage C, SARS/CoV 1+2:Lineage B) They DON’T even use ACE2 receptors to enter cells + have extra shorter Spikes:Hemagglutinin Esterase. We are comparing oranges 🍊 to grapefruits 3/
Read 22 tweets
Dr Nader K. Hijazi Profile picture
Dec 22, 2021
Mounting evidence confirming overall less severity with Omicron than Delta. This is definitely welcome & probably only good news coming out of this respiratory virus with unprecedented transmissibility. Even if same virulence would’ve been catastrophic 1/ medrxiv.org/content/10.110…
I expect a truly different phenotype (unique manifestations / symptoms) with predilection to invade upper airways more than lungs 🫁 with subsequent less systemic inflammation ➡️Illness➡️Death. 2/

med.hku.hk/en/news/press/…
It’s also clear: Mucosal immunity (ability to prevent upper airway infection) is low even > natural infection or vaccination, due to low & weak IgA response, which is our 1st line of defense for mucosal infection. This means unmitigated infectiousness 3/
Read 10 tweets

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