Humoral Immunity to HIV-1:

Lethal Force or Trojan Horse?
  • Peter L. Nara


The emerging evidence that specific genomic clades of HIV-1 are improving their fitness for efficient transmission via mucosal surfaces, i. e., heterosexual routes (Cohen, 1995; Osborn, 1995; Mastro et al., 1994), is disturbing and serves as an important backdrop for this book and a discussion of the role of humoral immunity. The evolution to improved fitness for mucosal transmission does not come as a surprise to those in the comparative lentivirus field, because the animal lentiviruses are as capable of broad transmission spectrum as one finds for enveloped RNA viruses (reviewed in Nara, 1988; Nara et al., 1991). These viral pathogens can assume either a cell-free or a cell-associated state, as dictated by the social and reproductive behaviors of the species. Because of genomic plasticity, primitive retroviral ancestry, and likely evolution with the vertebrates’ innate and adaptive immune systems, various aspects of humoral host defenses may have been exploited by the virus. Insights gained over the past few years now contribute to a more complete picture and understanding of so-called “humoral immunity,” which includes both nonclonal, innate, or nonadaptive immune system and the clonal, acquired (i. e., specific), or adaptive immune system. Together, these complementary defense systems must communicate to protect infectious nonself from noninfectious self. This is accomplished through similar structural/ functional forms of nonclonal and clonal inducible soluble host defense molecules (Janeway, 1992) by providing a continuous antimicrobial state during the period of initial infection and subsequent colonization of the host. These two defense systems now appear to be more inextricably linked in their induction than previously appreciated. Thus, depending on which effect or arms are activated, and in what order, may influence the establishment of conventional T- and B-cell-type immunity.


Human Immunodeficiency Virus Human Immunodeficiency Virus Type Seminal Plasma Humoral Immunity Envelope Glycoprotein 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • Peter L. Nara
    • 1
  1. 1.Laboratory of Tumor Cell Biology, Division of Basic SciencesNational Cancer Institute, National Institutes of HealthFrederickUSA

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