Table 2.
Potentiation of the ACV anti-HIV-1 activity by ribavirin in human tonsillar tissuesa
| Condition | ACV concn (μM) | HIV-1 replication [median p24gag (IQR)]b | % inhibitionc |
|---|---|---|---|
| Ribavirin (10 μM) | |||
| 0 | 7,379 (4,135–10,737) | NA | |
| 0.3 | 5,020 (3,220–8,837) | 18.3 ± 16.8 | |
| 3 | 2,284 (1,426–4,497) | 65.9 ± 17.0 * | |
| 10 | 1,327 (1,098–1,807) | 91.8 ± 7.5** | |
| No ribavirin | 0 | 8,228 (3,714–12,357) | NA |
| 0.3 | 8,528 (5,844–12,112) | 6.1 ± 11.7 | |
| 3 | 5,869 (3,554–8,257) | 41.3 ± 25.2 | |
| 10 | 3,234 (1,554–5,489) | 65.2 ± 17.6 |
For each condition, 27 tonsillar tissue blocks from each of n donors were inoculated with X4LAI.04 and treated for a 12-day period with 1, 3, or 10 μM ACV in the absence or presence of 10 μM ribavirin.
Median cumulative p24gag release (pg/ml) in culture supernatant of infected tissues. n = 10 for all data points except for 10 μM ACV, where n = 6. IQR, interquartile range.
Percentage (mean ± SD) of inhibition of HIV replication is defined as [1−(RACV/RCtl)] × 100, where RACV and RCtl are the amounts of p24gag accumulated in the medium over a 12-day culture period in ACV-treated cultures and in donor-matched untreated ACV cultures, respectively.
, P value of < 0.05 for HIV-1LAI.04 inhibition in the absence versus in the presence of 10 μM ribavirin at 3 μM ACV.
, P value of < 0.05 for HIV-1LAI.04 inhibition in the absence versus in the presence of 10 μM ribavirin at 30 μM ACV. NA, not available.