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/
• • •
Missing some Tweet in this thread? You can try to
force a refresh
➡️ A NEW study finds Metformin could prevent a form of acute myeloid leukemia (AML) in people at high risk of the disease.
Researchers investigated how metformin could prevent abnormal blood stem cells w/ genetic changes from progressing to AML 1/
Metformin impacts mitochondrial metabolism, & these pre-cancerous cells need this energy to keep growing. By blocking this process, researchers stop the cells from expanding & progressing towards AML, whilst also reversing other effects of mutated DNMT3A gene 2/
Thanks to recent advances, individuals at high risk of AML can be identified years in advance using blood tests and blood DNA analysis, but there's no suitable treatment that can prevent them from developing the disease. 3/
It has been reported that repeated administration of some COVID vaccines induces high IgG4 levels.
New research revealed a surprising IgE anti-RBD response after both natural infection & several SARS-CoV-2 vaccines. 1/
Presence of IgG4 & IgE in COVID-19 suggests that the virus may induce an “allergic-like” response to evade immune surveillance, leading to a shift from Th1 to Th2 cells, which promotes tolerance to the virus & potentially contributes to chronic infection & may be LongCovid 2/
An increase in IgG4 levels is typically associated w/ immunological tolerance & develops after prolonged exposure to antigens. While tolerance to an allergen benefits the host in Allergen Immunotherapy, in viral infection, it enables viral persistence rather than clearance 3/
Cells are swapping their mitochondria. What does this mean for our health?
Researchers are studying why Mitochondria, the energy factories are moving between cells and whether the process can be harnessed to treat cancer and other diseases. 1/.
It turns out that mitochondria can actually be transferred to other cells if needed.
Mitochondria move between different cells in 3 ways-through nanotubes, in extracellular bubble-shaped vesicles, or by free floating through the blood. 2/
How mitochondria are getting around is largely settled, but what’s less clear is why. Researchers are learning that the process is often a form of cellular damage control. 3/
SARS-CoV-2 has been widely reported to cause retinal pathological changes and to infect the embryonic retina. The infection of host cells by SARS-CoV-2 is primarily mediated through spike (S) protein, which also plays a crucial role in the pathogenesis of SARS-CoV-2. 1/
Spike protein exposure was studied in human embryonic stem cell-derived retinal organoids (hEROs) at various stages of retinal development. Immunofluorescence, RNA sequencing, and RT-PCR were used to determine how S protein exposure affects retinal development early and late 2/
The results showed that ACE2 and TMPRSS2, the receptors facilitating SARS-CoV-2 entry into host cells, were expressed in hEROs. Exposure to the S protein induced an inflammatory response in both the early and late stages of retinal development in the hEROs. 3/
Researchers have identified a new set of genes that contribute to the risk of Parkinson's disease (PD), which opens the door to previously untapped drug targets for treating PD.
PD is the 2nd most common neurodegenerative disease after Alzheimer's disease. 1/
A longstanding mystery in PD has been why some people carrying pathogenic variants that increase their risk of PD go on to develop the disease, while others who also carry such variants do not. The prevailing theory has suggested additional genetic factors may play a role 2/
The researchers used a genome-wide CRISPR interference screen to silence each of the protein-coding human genes in cells and identified those important for PD pathogenesis. 3/
A new study finds certain bacteria living in nose (nasal microbiome) may influence how likely someone is to get a COVID-19 infection. These bacteria can change crucial proteins the virus needs to enter human cells, explaining why some people are more susceptible to COVID 1/
Post-infection ACE2 and TMPRSS2 expression in the upper respiratory tract has been linked to increased disease severity among adults, and higher post-infection ACE2 expression has been linked to increased secondary transmission among adults,and risk of infection in children. 2/
In this study, elevated nasal ACE2/TMPRSS2 expression was associated with 3.6-fold increased risk of contracting COVID-19 compared to those with no detectable levels of ACE2 or TMPRSS2. 3/