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. 2004 Oct;48(10):3918–3927. doi: 10.1128/AAC.48.10.3918-3927.2004

TABLE 2.

Drug susceptibilities of HCMV strains resistant to BDCRB and maribavir

Compound IC50 (μM) in plaque reduction against the following virusesa:
IC90 (μM) in yield reduction against the following virusesb:
Towne D10 r56 C4 AD169 2916
853 24 ± 2 56 ± 1*c 51 ± 3* 56 ± 2* NDd ND
1049 0.61 ± 0.10 4.6 ± 0.3* 5.3 ± 0.4* 25 ± 5* ND ND
1311 0.66 ± 0.42 0.54 ± 0.16 0.81 ± 0.08 0.95 ± 0.18 0.82 ± 0.10 0.70 ± 0.18
GCV 13.3 ± 1.5 12.7 ± 1.2 13.3 ± 0.6 12.0 ± 5.0 1.2 ± 0.4 1.5 ± 0.3
BDCRB 1.0 ± 0.1 11.8 ± 0.8* 8.8 ± 0.7* 37.7 ± 2.5* 0.36 ± 0.12 0.38 ± 0.05
Maribavir ND ND ND ND 0.19 ± 0.09 57 ± 3*
a

Inhibition of HCMV plaque formation was measured by using at least six drug concentrations ranging from 100 to 0.05 μM. Data are presented as the means±SDs of IC50s determined in at least triplicate. HCMV strains D10, r56, and C4 were derived from Towne (wild-type strain) (described in references 24 and 45). D10 bears a mutation in UL89 (D344E), r56 contains a mutation in UL56 (Q204R), and C4 has both mutations.

b

Inhibition of HCMV titer production was measured at eight drug concentrations ranging from 100 to 0.05 μM. Data are presented as the means±SDs of IC90s determined in at least quadruplicate. HCMV strain 2916r was derived from AD169 (wild-type) (described in reference 6). Strain 2916r contains a mutation in UL97 (I397R).

c

*, P < 0.005 as determined by the Student's t test function of Microsoft Excel.

d

ND, not determined.