O'Brien W J, Piotrowski K, Taylor J L
Department of Ophthalmology, Medical College of Wisconsin, Milwaukee, USA.
Intervirology. 1995;38(5):249-55. doi: 10.1159/000150447.
Interferon-alpha (IFN-alpha) combined with acyclic guanine analogs synergistically inhibits replication of herpes simplex virus type 1. IFN-alpha treatment influenced the metabolism of exogenously supplied nucleobases and nucleosides in a manner expected to contribute to synergistic activity. IFN-alpha treatment of infected human cornea stromal cells or Vero cells significantly reduced steady-state levels of acid soluble metabolites of thymine, as well as thymidine, that accumulate early during virus replication but did not affect metabolism of thymine and thymidine in uninfected cells. IFN-alpha treatment significantly reduced the ability of uninfected cells to accumulate acid-soluble metabolites from guanine, but not guanosine. The effects of IFN-alpha on nucleobase/nucleoside metabolism could contribute to synergistic antiviral activity by reducing the accumulation of thymidine/thymine metabolites and decreasing the guanine taken into cells.
α干扰素（IFN-α）与无环鸟嘌呤类似物联合使用可协同抑制单纯疱疹病毒1型的复制。IFN-α治疗对外源性供应的核碱基和核苷的代谢产生影响，其方式有望促进协同活性。用IFN-α处理受感染的人角膜基质细胞或Vero细胞，可显著降低胸腺嘧啶以及胸苷的酸溶性代谢产物的稳态水平，这些代谢产物在病毒复制早期积累，但不影响未感染细胞中胸腺嘧啶和胸苷的代谢。IFN-α治疗显著降低了未感染细胞从鸟嘌呤而非鸟苷中积累酸溶性代谢产物的能力。IFN-α对核碱基/核苷代谢的影响可能通过减少胸苷/胸腺嘧啶代谢产物的积累以及减少进入细胞的鸟嘌呤来促进协同抗病毒活性。
