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. 2022 May 21;19:9. doi: 10.1186/s12977-022-00593-5

Table 1.

Virion incorporation of PSGL-1 and gp120 in a panel of clinical and laboratory virus isolates

Virus Isolate Clade Co-receptor usage Input virus (pg) Captured Virus Ratio (PSGL-1:gp120)
PSGL-1% of input (%) gp120% of input (%)
HIV-1 92UG037 A R5 3113 11 8 1.4
HIV-1 BaL B R5 3793 75 37 2.0
HIV-1 ADA B R5 8544 81 33 2.5
HIV-1 JRFL B R5 565 56 11 5.2
HIV-1 IIIB B X4 7068 35 79 0.4
HIV-1 07USLD B X4 6492 22 23 1.0
HIV-1 07USLR B X4 6035 16 20 0.8
HIV-1 92HT599 B R5X4 2101 66 26 2.5
HIV-1 93UG065 D X4 7577 76 56 1.4
HIV-1 93TH057 E R5 4642 44 8 5.5
HIV-1 CMU06 E X4 4026 31 4 7.2
HIV-1 97BR019 F R5X4 9629 31 2 17.5
HIV-1 PV PSGL-1Low B R5 35,000 19 1 13.5
HIV-1 PV PSGL-1Med B R5 35,000 76 0 172.5
HIV-1 PV PSGL-1High B R5 35,000 96 0 302.4
SIV smE660.307 R5 18,035 35 6 5.9
SIV mac251.745 R5 13,044 36 3 11.3

All viruses were produced in activated primary human PBMC, except for the HIV-1 pseudoviruses (PV; produced in HEK293T cells), which are displayed here as controls. The level of virion incorporation was determined by measuring the amount of captured virus by immunomagnetic beads armed with anti-PSGL-1 or anti-gp120 mAbs. Bead-associated virus was lysed and captured virus was quantified by readout of p24Gag for HIV-1 (or p27Gag for SIV). All clinical isolates were minimally passaged in vitro