Table 3 Summary of effects of each mutation on EEEV HS or receptor interactions

From: Three positively charged binding sites on the eastern equine encephalitis virus E2 glycoprotein coordinate heparan sulfate- and protein receptor-dependent infection

 

WT

71–77

84–119

156–157

SINV/EEEV CHO-pgsA-745 infectivity relative to CHO-K1 infectivity

6.4 ± 1.1%

122.8 ± 12.7%

8.2 ± 2.5%

85.4 ± 21.7%

SINV/EEEV heparinase II infection sensitivity

+++

+++

+++

SINV/EEEV heparin binding affinity (KD apparent)

3.5 ± 0.8 nM

132.8 ± 57.6 nM

5.1 ± 0.6 nM

163.3 ± 200.6 nM

SINV/EEEV susceptibility of infection to increased NaCl

+++

++

++

EEEV Genome:BHK PFU (Fold-Change to WT)

1

89.5

1.8

298.1

SINV/EEEV K562-VLDLR infectivity/VLDLR LA(1-2)-Fc neutralization

+++/+++

+/+

++/+++

+/−

SINV/EEEV VLDLR LA(1-2)-Fc binding affinity (KD apparent)

4.3 ± 1.4 nM

1.1 ± 0.4 nM

5.9 ± 1.4 nM

ND

Mouse AST sc. infection with EEEVs

4.1 ± 0.5

5.2 ± 0.5

3.7 ± 0.2

6.2 ± 0.7

Mouse mortality ic. infection with SINV/EEEV chimeras

60%

0%

20%

0%

VLDLR LA(1-2)-Fc in vivo protection from infection with EEEVs

+++

++

++

Mosquito midgut EEEV infectivity

+++

+

++

  1. Plus and minus signs represent a subjective ranking of the relative magnitude of each phenotype (− = no activity, + − +++ represents a continuum from low to high magnitude). ND not determined, due to low binding, AST average survival time, sc. subcutaneous, ic. intracranial.