Mechanisms of human immunodeficiency virus type 1 inhibition by hydroxyurea

被引：0

作者：

Lori, F ^{[1
]}

Lisziewicz, J ^{[1
]}

机构：

[1] RIGHT, Washington, DC USA

来源：

JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS | 1999年 / 13卷 / 03期

关键词：

HIV-1; hydroxyurea; mechanisms of action; virologic; immunologic;

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Virus life cycles depend on cellular factors. Therefore, targeting cellular in combination with viral enzymes could be an effective control in virus replication. In contrast to viral proteins, cellular proteins are not prone to mutations; therefore, viral escape is not expected from drugs inhibiting cellular factors. Hydroxyurea inhibits the cellular enzyme ribonucleotide reduetase, thus reducing DNA synthesis. Furthermore, this drug potentiates the activity of nucleoside analogues, inhibits the escape of A-analogue resistant mutants, and increases the phosphorylation of T-analogues. Besides its antiviral activity, hydroxyurea effects the immune system by decreasing immune activation, inhibiting the expansion of CD8 cells and the depletion of CD4 cells. Hydroxyurea has been used in medicine for 40 years, is well tolerated, and it is the least expensive available anti-HIV-l drug. These characteristics make hydroxyurea a primary candidate for use in combination therapies for the treatment of HIV-1 infection.

引用

页码：176 / 180

页数：5

共 40 条

[1] Long-term exposure to zidovudine affects in vitro and in vivo the efficiency of phosphorylation of thymidine kinase [J].