I'd like to detail exactly why I think Dr. Gottlieb's prediction is
 off, but not entirely wrong, and what strains I think may be faced this
 winter.  His premise that Delta spreads so rapidly that it will 
eventually burn itself out, perhaps even before winter, is very 
plausible and even likely.  Note that summers will favor strains with 
better transmissibility, while winter will favor strains with better 
immune evasion, due to inoculum levels varying with temperature.
It's
 the idea that cross-reactivity to anti-Delta antibodies will confer 
broad resistance to other strains, and thus the end of the pandemic, 
that I disagree with.
Depending
 on how fast Delta mutates relative to how fast it spreads, it may not 
even be a progenitor of the next major strain.  I would say the odds 
depend on recombination and the localization of existing mutations.  If 
its increased transmissibility is due mostly to its increased viral load
 in the nasal passages, it is likely tied to proteins other than S(see N
 and nsp6 in particular, discussed in this paper).  A putative 
recombination event with a strain with a different S gene would greatly 
increase the chance of Delta being the basis for the next major strain.
This
 paper supports the idea that recombination is the major driving force 
in the evolution of SARS-CoV-2.  However, many case studies have also 
demonstrated extremely rapid intra-host evolution in protracted 
infections, particularly in immunocompromised individuals.  This is 
obliquely mentioned in the paper, but they suggest that it would have 
had to occur on multiple continents, thinking it thus unlikely.  I don't
 think it's so far-fetched: it's happened in multiple individuals in 
single countries.  Recombination would have had to have happened 
multiple times in a short time frame and few of the accumulated 
mutations would be novel.
I
 like their MJN approach, and it does tilt the scales towards 
recombination in widely distributed strains, though each could remedy a 
hard polytomy.
Regardless,
 the S genes from other candidate strains following a different 
haplotype, not likely to be strongly cross-reactive with Delta, 
with a phenotype more marked by immune evasion may be more likely winter
 wave candidates than Delta.  The 
highly efficacious syncytia of Delta result largely from P681R, so a 
candidate strain
might be identified by S:E484K, N501Y, and P681H, and that includes 
B.1.621.  B.1.621 also has R346K for added evasion.
The failure of A.30 is peculiar to me, and may be due to missing D614G, as the rest of the virus looks quite serious.
Anyway,
 strains with the above haplotype have been doing quite well for 
themselves; their success has been concealed by the enormous spike in 
Delta prevalence.  Presuming that Delta burns itself out as Gottlieb 
suggests, they may abruptly become dominant on their own, or their S 
genes may be carried forward in a Delta shell through recombination.
Such
 recombination would create an additional wave and a worse scenario, 
creating a rapidly spreading strain that is also immunoevasive that 
should burn itself out again, but not before taking a lot of hosts out 
with it.  This is discussed in detail in "Recombination is the likely 
source for the rapidly expanding variants".
Whether that happens or not, we would be 
left with some other antigenically distant strain to take the reins, or 
more probably a resurgence of an antigenically drifted Delta with its own S gene as anti-Delta
 antibodies fade.
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