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Different Antiviral Potencies of BV‐araU and Related Nucleoside Analogues against Herpes Simplex Virus Type 1 in Human Cell Lines and Vero Cells
Author(s) -
Machida Haruhiko,
Nishitani Makiko,
Suzutani Tatsuo,
Hayashi Kozaburo
Publication year - 1991
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1991.tb01618.x
Subject(s) - vero cell , herpes simplex virus , biology , cell culture , virology , thymidine , nucleoside , virus , fibroblast , nucleoside analogue , cytotoxicity , potency , microbiology and biotechnology , in vitro , biochemistry , genetics
Antiviral potencies against herpes simplex virus type 1 (HSV‐1) of 1 ‐β‐ D‐arabinofuranosyl‐ E ‐5‐(2‐bromovinyl)uracil (BV‐araU) and ten other nucleoside analogues in human embryonic lung fibroblast (HEL) cells were compared with those in Vero cells. 5‐Halogenovinylarabinosyluracils, highly active in HEL cells, were inactive against all three laboratory‐stocked strains of HSV‐1 but exerted moderate antiviral effects on three clinical isolates in Vero cells. The reduction in anti‐HSV‐1 potencies of other representative nucleoside analogues in Vero cells was much less than those of 5‐halogenovinylarabinosyluracils. However, significant antiviral potencies of BV‐araU against laboratory strains were observed in other human and monkey fibroblast cells including an immortalized cell line. Significant enhancement of antiviral activity of BV‐araU against a laboratory strain and a clinical isolate was demonstrated in Vero cells by the addition of 0.1 μM aminopterin or FUdR, an inhibitor of thymidylate synthesis. The potentiated anti‐HSV‐1 activity in Vero cells was comparable to the potency in HEL cells without the inhibitor. These results suggested that high activity of thymidylate synthesis and a large thymidylate pool size in Vero cells seem to be related to loss of anti‐HSV‐1 potency of BV‐araU. Original tissue type, species, and the immortality may not be responsible for the reduced antiviral activity of BV‐araU in Vero cells.

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