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Another Leap in HIV Research

Thomas R. O'Brien, MD, MPH; James J. Goedert, MD

JAMA. 1998;279:317-318.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Advances in medicine and public health frequently occur in leaps rather than increments. For example, new therapeutic regimens that dramatically reduce viral replication,¹ combined with human immunodeficiency virus type 1 (HIV-1) RNA assays that measure circulating virus and predict the clinical course of HIV-1 infection,² have led to marked decreases in mortality from the acquired immunodeficiency syndrome (AIDS) in the United States.³ Equally dramatic strides have recently been made in our understanding of how HIV-1 enters cells and how human genetic variability affects susceptibility to infection and clinical prognosis.

Chemokine receptors are essential coreceptors for HIV-1 cell entry. This insight stemmed from 2 remarkable studies^4-5 addressing seemingly unrelated, long-standing questions of HIV-1 pathogenesis. Although it was postulated years ago that soluble factors secreted by lymphocytes might suppress HIV-1 replication, the identity of such factors was unknown until Cocchi et al⁴ found . . . [Full Text of this Article]

From the Viral Epidemiology Branch (Dr O'Brien), and the Division of Cancer Epidemiology and Genetics (Dr Goedert), National Cancer Institute, US Public Health Service, US Department of Health and Human Services, National Institutes of Health, Bethesda, Md.

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