Have we reached to the peak of 2nd #Covid wave in India? May be, yes! Its already 2.5 months in to it. Most badly affected countries peaked within 1.5-3 months of onset of a new surge. Is it too early to comment? 1/
More interesting would be to see which way our curve goes: the UK/Israel or the US way! While both UK/Israel took 1.5-2 months to flatten their curves w/ strict lockdowns & aggressive vaccination, US had a long plateau (>3.5 months) 2/
However, there is heterogeneity in caseloads: While states like MH, UP, CG, PB, DL are showing ⬇️ in case load, some southern & eastern states (KA, KL, AP, TN, WB, ) still reporting cases in high numbers! What is driving Covid in these states? 3/ indiatoday.in/coronavirus-ou…
Different variants (VOC) are circulating in diff states of India. While it is #B1617 is in MS & neighboring states, #B117 in PB, DL & northern states, Delhi & #B1618 in WB & eastern states outbreak.info/situation-repo… 4/
Now, a new variant having #N440K spike substitution is believed to be behind the sudden rise of cases in southern India, particularly in KA, KL, AL & Telangana. Some believe it is believed to be 15 times more lethal than the earlier ones 5/ biorxiv.org/content/10.110…
So, what lies in store for #India? The few key factors that may extend India's suffering for a prolonged period:
1-lack of strict #lockdowns: having halfway yo-yo lockdowns are not the answer!
2-sluggish #inoculation drive: still only 2% of the population received 2-doses! 6/
3-rampant circulation of #variants: not sure which one is the main driver!
4-limited #sequencing: only 1% of isolates sequenced!
5-modestly efficacious #vaccines: unlike the other 3 countries
6-lack of #effectiveness data on currently employed vaccines: so, driving blindly! 7/
What could be the saving grace? Hoping the rapid descent follows the explosive ascent! And the virus, mutating at a staggering pace, might be heading for an evolutionary cliff all on its own. Amen! 8/ bbc.com/future/article…
One interesting thing to note: All the three countries had 3 waves, the last surge the severest!
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COVID-19 may be, in part, a mitochondrial disease.
➡️ A Cambridge review shows SARS-CoV-2 disrupts mitochondrial function in lung cells—driving inflammation and worsening pneumonia.
➡️ Emerging studies suggest even after the active infection is resolved, residual viral proteins, particularly SARS-CoV-2 spike protein, may linger and continue to cause damage to the mitochondria by increasing oxidative stress and disrupting energy metabolism, offering a plausible mechanism for #LongCOVID. 1/
H/T: @CatchTheBaby
COVID-19 is not just viral—it’s metabolic.
SARS-CoV-2 hijacks mitochondria →
↓ Energy production
↑ Inflammatory signaling
A key pathway worsening lung injury. 2/
Mitochondria may link acute COVID → #LongCOVID.
Viral disruption of mitochondrial function can persist, sustaining oxidative stress and immune dysregulation even after infection. 3/
New study shows SARS-CoV-2 directly damages heart cell mitochondria—key energy engines—offering a mechanistic link to #LongCOVID cardiovascular symptoms. 1/
#LongCOVID may be a mitochondrial disease: electron microscopy reveals structural damage & myofilament breakdown in cardiomyocytes. 2/
Biopsies from LongCOVID patients confirm myocarditis with mitochondrial disruption—mirrored in infected animal models. Strong biological plausibility for persistent cardiac symptoms. 3/
New research finds that SARS-CoV-2 spike protein can persist in the gut of people with #LongCOVID, even months after infection.
➡️ This persistent viral antigen may drive ongoing immune changes in intestinal tissue.
➡️ Scientists detected viral spike RNA and protein in colon and ileum biopsies from Long COVID patients.
➡️ In these regions, genes linked to inflammation, immune dysfunction, and tissue stress were altered. 1/
Persistent spike-positive areas in the colon showed increased immune cell activity, including:
• Macrophages
• Plasma cells
• Regulatory T cells
Suggesting an active local immune response in the gut.
➡️ Researchers also found disrupted expression of key immune-signaling genes, indicating impaired immune coordination and chronic inflammation in gut tissues. 2/
SARS-CoV-2 persistence is a proposed driver of Long COVID (LC), but the in-situ relationship between residual viral antigen and immune dysregulation remains poorly defined.
➡️ This NEW study provides robust evidence that persistent SARS-CoV-2 Spike protein detection in the gut is not immunologically inert.
➡️ Instead, it is actively associated with distinct, immune cell composition shifts and a dysfunctional pro-inflammatory transcriptional profile, supporting the hypothesis that retained viral antigen drives chronic immune dysregulation in tissue of LongCOVID subjects. 3/