This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on HighWire  • Citing articles on Web of Science (5)  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Peter C. Doherty, PhD, FRS

JAMA. 1995;274(13):1067-1068.

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

THE HUMAN immunodeficiency virus (HIV) pandemic has made us aware of the intimate relationships between viruses and the immune system. These human lentiviruses grow in lymphocytes of the CD4+ subset and are probably controlled, at least for a time, by the CD8+ effectors of cell-mediated immunity (CMI). When we discuss CMI-based strategies to limit HIV infection, the debate is framed by the efforts made over the past 20 years to understand the way that the major histocompatibility complex (MHC) glycoproteins function in viral immunity. This article places these efforts in historical context and, together with the accompanying article by Rolf Zinkernagel,¹ relates how our understanding of virus-specific CMI and the biological role of the MHC became intertwined.

BACKGROUND

In the early 1970s, the international effort on virus-specific CMI was minuscule. Most virologists had shifted their attention from whole-animal studies, in which virology and immunology approaches were inextricably linked, to . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Immunology, St Jude Children's Research Hospital, Memphis, Tenn.

Footnotes
Dr Doherty is the recipient of the 1995 Albert Lasker Basic Medical Research Award.

Reprint requests to St Jude Children's Research Hospital, 332 N Lauderdale, Memphis, TN 38105 (Dr Doherty).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?