Since its emergence in 1968, H3N2 has undergone a considerable number of mutations. It is, in a way the "Omicron" of HxNx viruses with several types :
- H3N2 HUMAN, which was the main strain this winter 2022/23 with in US (CDC) :
2) H3N2 SWINE, which evolved from H2N2 by antigenic shift, and caused the Hong Kong Flu pandemic of 1968 and 1969 that killed between one and four million people globally.
4) H3N2 CANINE, which was identified in Asia during the 2000s with a mutation that adapted from its avian influenza origins and was recently detected in US.
2) This first figure helps explain the first key mechanisms contributing to cognitive impairment in COVID-19 patients:
▶️ Direct viral entry and brain injury is shown in the first panel.
▶️ The role of hypoxia (lack of oxygen) in cognitive decline is depicted in the second panel
3) ▶️ The widespread systemic inflammation caused by COVID-19 is illustrated in the third panel.
For CHILDREN, the risk of LONG COVID after a SECOND INFECTION is 2.08 TIMES GREATER compared to the FIRST INFECTION. medrxiv.org/content/10.110…
2) Let's summarize first this study :
The researchers used medical records from 40 children's hospitals in the US between January 2022 and October 2023. They compared the risk of long-term issues in those with a second COVID-19 infection versus their first infection.
3) Results showed that children with a 2nd infection had a significantly higher risk of various long-term problems, including:
- Heart issues like inflammation and abnormal heart rhythms
- Changes in taste and smell
- Blood clots
- Kidney problems
- Fatigue and muscle/joint pain
What a "CLEVER" SARS-COV-2 virus !
... which induced a P812S mutation in a chronically ill individual, that is somewhat less pathogenic but enables the virus to infect a larger population. biorxiv.org/content/10.110…
2) This study looks at how a single mutation, called P812S, in the SARS-CoV-2 virus can have different effects. The P812S mutation was found in a person with a long-term COVID-19 infection.
3) The study found that the P812S mutation:
- Reduced the ability of the virus to enter cells and cause them to fuse together (form syncytia). This is linked to less severe COVID-19 disease.
- Helped the virus evade antibodies that target the fusion peptide region of the spike.
INSIDE a COVID-19 crashing WAVE (Nov. 2023 and Mar. 2024, coastal Kenya) 🌊
Fascinating information on variants, symptoms, reinfections, ...
Thanks @siamosolocani
for the study medrxiv.org/content/10.110…
2) The study examines the genomic and clinical epidemiology of a SARS-CoV-2 wave that occurred in coastal Kenya between November 2023 and March 2024. Key findings include:
- The wave was dominated by the XBB.2.3-like and JN.1-like Omicron subvariants ...
3) ... which were introduced through multiple independent events, primarily from North America and Europe.
- Genomic surveillance revealed at least 38 separate virus introduction events into the local population during this wave.
2) Here are the significant reductions in multiple key immune cell populations at 10 months after initial COVID-19 infection :
▶️ Total leukocyte (white blood cell) counts were reduced by 12%
▶️ Neutrophil counts were reduced by 11%
▶️ Monocyte counts were reduced by 10%
3) ▶️ Total lymphocyte counts were reduced by 14%
▶️ T cell counts were reduced, with CD4+ T cells down 16% and CD8+ T cells down 18%
▶️ B cell counts were reduced by 14%
▶️ Natural killer cell counts were reduced by 19%
How SARS-CoV-2 virus changed over 14 months in a patient with a weak immune system ?
The patient was first infected with the B.1.160 variant, then later got infected with the B.1.1.7 variant. The virus kept changing and evolving inside this patient's body biorxiv.org/content/10.110…
2) The virus mutated and recombined, creating new versions of itself. This allowed the virus to adapt and become better suited to the patient's body.
The study found that the virus evolved faster inside this patient compared to how it usually evolves in the general population.
3) This is because the patient's weak immune system allowed the virus to keep changing and trying out new mutations.
Some key mutations were found in genes like Spike, N, ORF9b, and nsp13. These mutations helped the virus evade the patient's immune system and replicate better.