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Examples of vaccine-induced enhancement of susceptibility to virus infection or of aberrant viral pathogenesis have been documented for infections by members of different virus families. Several mechanisms, many of which still are poorly understood, are at the basis of this phenomenon. Vaccine development for lentivirus infections in general, and for HIV/AIDS in particular, has been little successful. Consequently, vaccine-induced enhancement has been a major stumble block in the development of certain flavi-, corona-, paramyxo-, and lentivirus vaccines.. For vaccine-induced enhanced susceptibility to infection with certain viruses like feline coronavirus, Dengue virus, and feline immunodeficiency virus, it has been shown that antibody-dependent enhancement (ADE) plays an important role. Other mechanisms may, either in the absence of or in combination with ADE, be involved. Consequently, vaccine-induced enhancement has been a major stumble block in the development of certain flavi-, corona-, paramyxo-, and lentivirus vaccines. Also recent failures in the development of a vaccine against HIV may at least in part be attributed to induction of enhanced susceptibility to infection. There may well be a delicate balance between the induction of protective immunity on the one hand and the induction of enhanced susceptibility on the other. The present paper reviews the currently known mechanisms of vaccine-induced enhancement of susceptibility to virus infection or of aberrant viral pathogenesis.
Keywords: Vaccine, Enhancement, ADE, HIV, Lentivirus
Lentiviruses have infected several mammalian species including humans (human immunodeficiency virus-1 (HIV-1) and HIV-2), non-human primates (simian immunodeficiency viruses (SIV's)) and cats (feline immunodeficiency virus (FIV)), sometimes affecting a significant proportion of the host population (for reviews see , ). Despite their relatively wide distribution, the transmission of lentiviruses is generally not very efficient. After inoculation, the virus enters host target cells via interaction with one or more cellular receptors. For HIV-1, HIV-2 and SIV, CD4 is used as the primary receptor while chemokine receptors like CCR-5 or alternatively CXCR-4 are required as secondary receptor. Similarly, FIV enters its target cell using CD134 as a primary and CXCR-4 as a co-receptor. Interference with viral entry by vaccine-induced antibodies or antiviral therapy has been one of the major goals in the development of lentiviral intervention strategies. In spite