Progress on new vaccine strategies against chronic viral infections
Jay A. Berzofsky, … , Masaki Terabe, Igor M. Belyakov
Jay A. Berzofsky, … , Masaki Terabe, Igor M. Belyakov
Published August 16, 2004
Citation Information: J Clin Invest. 2004;114(4):450-462. https://doi.org/10.1172/JCI22674.
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Review

Progress on new vaccine strategies against chronic viral infections

Abstract

Among the most cost-effective strategies for preventing viral infections, vaccines have proven effective primarily against viruses causing acute, self-limited infections. For these it has been sufficient for the vaccine to mimic the natural virus. However, viruses causing chronic infection do not elicit an immune response sufficient to clear the infection and, as a result, vaccines for these viruses must elicit more effective responses — quantitative and qualitative — than does the natural virus. Here we examine the immunologic and virologic basis for vaccines against three such viruses, HIV, hepatitis C virus, and human papillomavirus, and review progress in clinical trials to date. We also explore novel strategies for increasing the immunogenicity and efficacy of vaccines.

Authors

Jay A. Berzofsky, Jeffrey D. Ahlers, John Janik, John Morris, SangKon Oh, Masaki Terabe, Igor M. Belyakov

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Figure 2

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Interactions of HIV envelope glycoproteins, CD4, and chemokine receptors...
Interactions of HIV envelope glycoproteins, CD4, and chemokine receptors CCR5 or CXCR4 trigger fusion and entry of HIV. These interactions determine critical regions of the HIV envelope glycoprotein against which neutralizing antibodies could be raised. After the envelope protein interacts with CD4 on the target cell (A and B), it undergoes a conformational change allowing its interaction with a chemokine receptor (C). This second interaction induces a further conformational change in the gp41 portion of the envelope glycoprotein that mediates the fusion event (D and E). Blockade of any of these three steps can prevent viral entry.