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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Rep 2021 ; 35 (13): 109292 Nephropedia Template TP
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Recurrent emergence of SARS-CoV-2 spike deletion H69/V70 and its role in the Alpha variant B 1 1 7 #MMPMID34166617
Meng B; Kemp SA; Papa G; Datir R; Ferreira IATM; Marelli S; Harvey WT; Lytras S; Mohamed A; Gallo G; Thakur N; Collier DA; Mlcochova P; Duncan LM; Carabelli AM; Kenyon JC; Lever AM; De Marco A; Saliba C; Culap K; Cameroni E; Matheson NJ; Piccoli L; Corti D; James LC; Robertson DL; Bailey D; Gupta RK
Cell Rep 2021[Jun]; 35 (13): 109292 PMID34166617show ga
We report severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike DeltaH69/V70 in multiple independent lineages, often occurring after acquisition of receptor binding motif replacements such as N439K and Y453F, known to increase binding affinity to the ACE2 receptor and confer antibody escape. In vitro, we show that, although DeltaH69/V70 itself is not an antibody evasion mechanism, it increases infectivity associated with enhanced incorporation of cleaved spike into virions. DeltaH69/V70 is able to partially rescue infectivity of spike proteins that have acquired N439K and Y453F escape mutations by increased spike incorporation. In addition, replacement of the H69 and V70 residues in the Alpha variant B.1.1.7 spike (where DeltaH69/V70 occurs naturally) impairs spike incorporation and entry efficiency of the B.1.1.7 spike pseudotyped virus. Alpha variant B.1.1.7 spike mediates faster kinetics of cell-cell fusion than wild-type Wuhan-1 D614G, dependent on DeltaH69/V70. Therefore, as DeltaH69/V70 compensates for immune escape mutations that impair infectivity, continued surveillance for deletions with functional effects is warranted.