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THE development of specific antiviral drugs that are minimally toxic to normal cells has ushered in a new era of antiviral therapy. The advent of this therapy is especially timely in the light of the threat to the lives of immunocompromised patients from cytomegalovirus infection,1 , 2 the increasing morbidity of recurrent genital herpes simplex infection,3 and most notably, the rising epidemic of the acquired immunodeficiency syndrome (AIDS), a lethal retroviral infection caused by human immunodeficiency virus type 1 (HIV-1).4 In theory, antiviral drugs work by interacting directly with the virus, with a viral-encoded enzyme or other protein, or with a cellular . . .
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A 1989 study studied this question.
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