P-selectin glycoprotein ligand-1 (PSGL-1/CD162) is incorporated into clinical HIV-1 isolates and can mediate virus capture and subsequent transfer to permissive cells

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)
Virus	Isolate	Clade	Co-receptor usage	Input virus (pg)	PSGL-1% of input (%)	gp120% of input (%)	Ratio (PSGL-1:gp120)
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-1^Low	B	R5	35,000	19	1	13.5
HIV-1 PV	PSGL-1^Med	B	R5	35,000	76	0	172.5
HIV-1 PV	PSGL-1^High	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

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