The Veesler Lab
@veeslerlab
Followers
6K
Following
1K
Media
343
Statuses
1K
Pathogen entry into cells, host immune responses & vaccine design: structural biology, protein design, virology & immunology @HHMINEWS @UWBiochemistry
Seattle, WA
Joined October 2014
RT @GuptaR_lab: Incredibly honoured to be taking up an exciting new chair of Global Health here at Cambridge and co-directorship of the Hon….
0
9
0
RT @jbloom_lab: @bblarsen1 @CaelanRadford @VUMC_Vaccines @veeslerlab The final version of our pseudovirus deep mutational scanning of the N….
0
4
0
RT @pdhsu: Delighted to see @arcinstitute research highlighted by Vox's Future Perfect 50 list!.
0
5
0
We found that even an antibody targeting the S N-terminal domain (S2L20) and preventing the receptor-binding domain from closing promotes S ratcheting and fusogenic triggering!. 5/6
1
6
13
In this manuscript, we dissect what makes a functional receptor from a mechanistic standpoint and shows that two key features to promote entry into cells are proper spatial/geometric organization & the ability to induce this ratcheting mechanism. 4/5
1
7
13
In 2019, we proposed w @coronalexington @axiong_x that coronavirus entry into cells involves a spike (S) molecular ratcheting mechanism & discovered that antibodies could functionally mimic the receptor by inducing these S conformational changes. 2/5.
1
4
16
Excited to share our latest work elucidating the mechanisms of coronavirus entry into cells!. Led by @Dr_MattMcCallum on our side in collaboration with Huan Yan's lab (TaiKang Center for Life and Medical Sciences). 1/5.
3
36
118
Collectively, these data indicate that receptor interference is a primary mechanism of PDCoV neutralization, inform immunity against deltacoronaviruses and will guide the design of vaccines for swine & human populations. 6/7
1
2
5
PD33 and PD41 escape profiles do not overlap, with the exception of substitutions to site G319, which are universally deleterious for receptor-binding affinity, and these 2 mAbs could thus be used as a cocktail with enhanced resistance to escape. 5/7.
1
1
3
For the 2 most potent mAbs (PD33 and PD41), most escape mutations led to dampening of gAPN-binding avidity, suggesting that they would not be tolerated due to reduced viral fitness. 4/7
1
1
3
During the review process, we added deep-mutational scanning data from @tylernstarr lab to identify mutations that escape binding of four neutralizing mAbs (PD17, PD20, PD33, and PD41) and two non-neutralizing mAbs (PD3 and PD8). 3/7.
1
1
4
The initial thread describing our @biorxivpreprint can be found here. 2/7.
PDCoV was shown to be able to use human APN for cell entry and was recently associated with multiple zoonotic transmission events in children with acute undifferentiated febrile illness. 2/15.
1
1
3
The peer-reviewed version of our study describing monoclonal antibodies (mAbs) inhibiting porcine deltacoronavirus, which jumped to humans multiple times recently, is now online. 1/7 .
1
11
32
@Dr_MattMcCallum is on the faculty job market. Catch him if you can! He is incredibly talented & innovative!. 9/9.
0
2
11
We show that the stabilization strategy we designed is broadly applicable to alpha-, beta-, and gamma-Herpesviruses, pointing to a shared fusion mechanism and paving the way to develop vaccines against these pathogens. 8/9
1
2
4
We determined a cryoEM structure of EBV gB, providing an atomic-level description of this key therapeutic target that had resisted structural characterization for several decades!. 7/9.
1
0
6
We leveraged recent breakthroughs in machine learning-guided protein design to stabilize the prefusion EBV gB ectodomain trimer and elucidate the mechanism of gB-mediated fusion. 6/9
1
0
4