Which arm is crucial for viral clearance & protection against #SARSCoV2? 1/
Early on in the #pandemic questions arose regarding how #SARSCoV2 is cleared during acute/primary infection & what aspects of the #adaptive immune were necessary and sufficient for protection from repeat infection 2/
Using mouse models of SARSCoV2,@BenIsraelow Rt al demonstrate that both humoral and cellular adaptive immunity contributes to viral clearance in the setting of primary infection 3/
Either convalescent mice, or mice that receive #mRNA vaccination are protected from both homologous infection & infection with a VOC, B.1.351 4/
Additionally, they conclude that protection is largely mediated by antibody response and not cellular immunity, and highlight the in vivo protective capacity of antibodies generated to both vaccine & natural infection @VirusesImmunity@SaadOmer3 5/
Another study on Rhesus #Macaques finds that T cells play a role in the recovery from acute #SARSCoV2 infections, their depletion does not induce severe disease, & T cells do not account for the natural resistance of rhesus macaques to severe #COVID19@fitterhappierAJ 6/
Neither primed CD4+ or CD8+ T cells appeared critical for immunoglobulin class switching, the development of immunological memory or protection from a second infection 7/
CD4, CD8, & CD4/8 depletion in Macaques prior and during infection did not affect disease course and only mildy attenuated viral clearance! 8/
The debate continues.....Difficult to write-off the importance of T-cells. This virus is weird. Need more studies before we dump cellular arm. What we know, a harmony between the two is needed for a successful immune response! 9/
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Can past COVID-19 weaken the body’s ability to fight tuberculosis?
➡️ A new study comparing immune responses to SARS-CoV-2 and Mycobacterium tuberculosis (MTB) suggests COVID-19 may dampen both antiviral and anti-TB immunity — even months later. 1/
Researchers tested immune cells from healthy individuals and COVID-19 survivors, both with and without latent TB infection (LTBI).
➡️ They stimulated the cells with SARS-CoV-2 Spike and MTB antigens and measured cytokine responses. 2/
Key finding:
➡️ People who recovered from COVID-19 showed significantly reduced inflammatory cytokines — IFN-γ, IL-2, IL-6, TNF-α — in response to both SARS-CoV-2 and MTB antigens.
➡️ Suggests prolonged immune downregulation after COVID-19. 3/
A new study comparing immune profiles months after COVID-19 vs influenza shows that SARS-CoV-2 leaves behind distinct and longer-lasting immune abnormalities — very different from what is seen after flu. 1/
Post-COVID patients showed increased CXCR3 and CCR6 expression across multiple lymphocyte populations.
➡️ Punjabi This means their immune system is still sending signals for cells to migrate into tissues (especially the lungs) months after infection.
In contrast, post-flu patients mainly showed a decrease in CCR4 on naïve T cells, monocytes, and dendritic cells — a very different and less persistent pattern.
➡️ Flu does not drive the same long-term immune activation. 3/
A new study provides some of the strongest evidence yet that mitochondrial dysfunction can directly cause #Parkinson’s disease, rather than being a consequence of neuron loss.
➡️ Researchers used a unique mouse model carrying a mutation in CHCHD2, a mitochondrial protein linked to a rare inherited form of Parkinson’s that closely mimics the common, late-onset form. 1/
Key Findings
➡️ Mutant CHCHD2 accumulates in mitochondria, making them swollen and structurally abnormal.
➡️ Cells shift away from normal energy production and develop oxidative stress due to buildup of reactive oxygen species (ROS).
➡️ Alpha-synuclein aggregation occurs after ROS rises, suggesting oxidative stress triggers Lewy body formation.
➡️ Human brain tissue from people with sporadic Parkinson’s showed CHCHD2 accumulation inside early alpha-synuclein aggregates, confirming relevance beyond the rare genetic form. 2/
Implications
➡️ This work maps a step-by-step causal chain:
CHCHD2 mutation → mitochondrial failure → metabolic shift → ROS buildup → alpha-synuclein aggregation → Parkinson’s pathology
➡️ It supports the idea that mitochondrial defects may underlie many forms of Parkinson’s, not just the inherited type.
➡️ Targeting oxidative stress, mitochondrial health, and energy pathways could offer new therapeutic strategies. 3/
New research in Cell Reports Medicine helps explain why women are more likely to develop #LongCOVID — and often experience more severe, persistent symptoms like fatigue, brain fog, and pain.
The key? Differences in the immune system, gut, and hormones. 1/
Researchers studied 78 people with LongCOVID (mostly mild initial cases) and compared them to 62 who recovered fully.
➡️ One year later, women with Long COVID showed clear biological differences — especially signs of gut inflammation and “leakiness.” 2/
The study also found anemia and hormone imbalances.
Women with LongCOVID had lower testosterone — a hormone that normally helps control inflammation.
➡️ Lower testosterone was linked to more fatigue, pain, brain fog, and depression. 3/
➡️ Long COVID isn’t one disease — it’s a complex web of immune, vascular, and metabolic dysfunctions.
From fatigue & brain fog to heart & lung complications, it stems from viral persistence, autoimmunity, and mitochondrial damage. 1/
Proposed mechanisms:
1️⃣ Persistent viral reservoirs or antigen remnants
2️⃣ Reactivation of latent viruses (e.g., EBV)
3️⃣ Immune dysregulation & autoimmunity
4️⃣ Endothelial injury and microclots
5️⃣ Gut microbiome imbalance
6️⃣ Mitochondrial dysfunction and energy metabolism impairment. 2/
Current management:
- largely symptomatic—rehabilitation, pacing, and supportive therapies.
-Emerging treatments: under study — antiviral drugs, immune-modulating agents, microbiome restoration, and mitochondria-targeted therapies.
-Vaccination: reduces risk and severity of LongCOVID. 3/