Table 3.

STAg-derived cyclophilin (C-18) inhibits infectivity of HIV-1 R5 strains


Virus

Clade

Coreceptor

Target cell

ID50, μg/mL
JR-CSF B (US) CCR5 PM1 0.4 
Ba-L   B (US)   CCR5   PM1   3.8  
92US657 B (US) CCR5 PBMC 2.1 
92BR003   B (Brazil)   CCR5   PBMC   2.7  
92BR017 B (Brazil) CCR5 PBMC 4.0 
92BR007   C (Brazil)   CCR5   PBMC   14.0  
98CN009 C (China) CCR5 PBMC 3.3 
98IN017
 
C (India)
 
CXCR4
 
PBMC
 
No inhibitor
 

Virus

Clade

Coreceptor

Target cell

ID50, μg/mL
JR-CSF B (US) CCR5 PM1 0.4 
Ba-L   B (US)   CCR5   PM1   3.8  
92US657 B (US) CCR5 PBMC 2.1 
92BR003   B (Brazil)   CCR5   PBMC   2.7  
92BR017 B (Brazil) CCR5 PBMC 4.0 
92BR007   C (Brazil)   CCR5   PBMC   14.0  
98CN009 C (China) CCR5 PBMC 3.3 
98IN017
 
C (India)
 
CXCR4
 
PBMC
 
No inhibitor
 

PM1 cells were infected with the R5 virus (BA-L, JR-CSF) (100 TCID50 per well). PBMCs were stimulated with PHA-P (0.25 μg/mL) and IL-2 (20 U/mL) for 3 days and were then infected with primary isolates (100 TCID50 per well). C-18 protein (at serial 3-fold dilutions) was preincubated with the cells for one hour at 37°C before addition of the virus (5 replicate per group). The virus was washed away after 2 days. Supematants were collected every 2 days and assayed for p24 activity. The 50% viral inhibition dose was calculated according to Reed and Muench as described by Shibata et al. 16  No inhibition was observed with human cyclophilin.

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