The duration of immunity in #SARSCoV2 infected people remains unclear. Recent studies have estimated that the correlate of 50% protection from re-infection was 20% of the mean convalescent #NAbs titre 2/
The sera collected from a cohort of 125 individuals with RT-PCR confirmed SARSCoV2 infections up to 386 days after symptom onset. In the subset of 65 sera collected from day 151 to 386 after symptom onset, all remained positive in PRNT50 3/
Since Ab waning follows a bimodal pattern with slower waning > day 90 after illness, lines of decay fitted to 115 sera from 62 patients collected beyond 90 after symptom onset & estimate that #PRNT50 Ab will remain detectable for around 1,717 days after symptom onset 4/
Break-up: 1,574 days for mild infections & 2,709 days for severe infections. However, because the slope of decline was not significant for symptomatic patients, these may be under-estimates 5/
Peak PRNT titres in mildly symptomatic #children did not differ from those in mildly symptomatic adults but these antibody titres appear to wane faster in children. 6/
Further, even if protection from re-infection may wane beyond 2 years after infection, immune memory for both B & T cell compartments are likely to remain and will lead to rapid increase in NAbs upon re-infection, thus conferring even longer protection from severe disease 7/
Can these results from natural infection be directly extrapolated to results from #immunization? No. Since, on one hand, #mRNA vaccines elicit NAbs titres markedly higher that those obtained from natural infection, some vaccines produce significantly low NAbs titers 8/
The generation of #memory B cells & long-lasting plasma cells resident in bone marrow following vaccination may differ markedly with that arising from natural infection & this may be reflected in differences in rates of antibody waning and in the correlates of protection 9/
Interestingly, the breadth of cross neutralization appears to increase over time following natural infections but whether then same will occur after vaccination remains to be understood 10/
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A recent #Chinese study shows that the viral loads in the #Delta infections were ~1000 times higher than those in the earlier 19A/19B strain infections on the day when viruses were firstly detected 1/
#Delta not only had a shorter incubation period but also has a shorter latent period. So, the time difference stayed the same but with much higher viral load. That's terrible & explains near-vertical waves 2/
Because it binds & replicates faster, #Delta creates a higher viral load which triggers symptoms in a host much faster 3/
Like all viruses, #SARSCoV2 will continue to evolve. But it has limited number of moves available. It seems it is near to its ‘end game’. There is just not a lot of space for the spike to continue to change in ways that allow it to evade Abs but still bind to its receptors 2/
#Substitutions that allow the virus to resist antibodies will probably also decrease its affinity for #hACE2. This is exactly what we have seen with #DeltaPlus 3/
Can #SARSCoV2#variants fully evade #vaccine induced protection? Or even natural protection?
The rapid emergence of too many different #variants shows that the virus is struggling to survive! That is why it’s changing so fast, probably, to prolong its stay in human bodies 1/
Though #vaccines may not be working perfectly against some #VOCs, but those fully vaccinated are protected against severe disease & death. No VOC can completely evade the vaccine induced protection, especially against severe disease & death! Why?.......... 2/
The #variants do not have changes in T-cell epitopes because when you are infected with a variant that evades an antibody, that variant can go to someone else and evade their antibody too. So it spreads through the population.... 3/
Do children produce different types of #antibodies(Abs) against #SARSCoV2 than adults? 1/
Yes, children mostly produced Abs aimed at #Spike protein, which the virus uses to enter cells. Adults generate similar Abs, but also develop Abs against the #Nucleocapsid protein, which is essential for viral replication 2/
#Nucleocapsid protein is typically released in significant quantities only when a virus is widespread in the body.
What does it mean? The kids lacked nucleocapsid-specific Abs, which suggests that they aren’t experiencing widespread infection. 3/
Can a respiratory #virus infection confer #immunity against the other #respiratory virus? A much-debated issue in the virus immunology for many decades. What is the probable immune mechanism & does it indeed exist? What is the evidence for & against this hypothesis? 1/
It is hypothesized that a respiratory virus infection confers immunity against the same and other respiratory viruses for a short time, perhaps a few weeks. This immunologic mechanism, known as #heterosubtypic ‘temporary non-specific immunity’ 2/
This immune protection is associated with activation of the innate immune response to viral infection mediated by the release of Type I #interferons (IFN) & other cytokines that have broad protective effects against a range of viruses 3/
‘#Spike protein’ is the major target of #NAbs in infected/vaccinated people. The prefusion conformation of the Spike represents the most relevant target because Abs can successfully interfere w/ infection only if they prevent binding to target cells or prevent fusion itself 1/
Various approaches are adopted to express ‘#Spike’ protein in vivo, such as nucleic acid structures & virus vectors. Alternatively, other vaccine platforms like recombinant protein particles & inactivated vaccines can directly deliver this protein 2/
Most structural studies of the wild-type spike protein exhibited one #RBD in the 'open' conformation. By contrast, 2 or 3 RBDs were observed in the open conformation in the more infective #D614G mutant--the RBD #conformation plays a vital role in the infectivity of SARSCoV2 3/