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Antibody dependent enhancement (ADE) occurs when antiviral antibodies enhance viral entry into host cells, leading to increased infectivity in the host cells.

ADE in dengue fever

The most known example of ADE occurs during dengue infection. There are four serotypes of the dengue virus, numbered from 1 to 4. ADE occurs when a patient suffering from a dengue infection is infected with a different serotype of the dengue virus. These patients have severe clinical outcomes and high viremia compared with other dengue sufferers.

Dengue virus (DENV) is a single-stranded positive-polarity RNA virus of the Flaviviridae family. DENV causes a wide range of diseases in humans, from a self limited dengue fever (DF) to a life-threatening syndrome (dengue hemorrhagic fever [DHF] or dengue shock syndrome [DSS]).[1] It is estimated that up to 100 millions individuals are infected with DENV annually.[2] DENV is constituted by four antigenically different serotypes (DENV1-4)[2], and if infection induces long-life protection against the infecting serotype, it gives only a short time cross protective immunity against the other types.[3] Moreover, if first infections cause mostly minor disease(DF) or few cases of severe diseases (DHF/DSS) in children, secondary infections has been reported to cause severe diseases in both children and adults.[3]

In 1997, 205 cases of DHF/DSS occurred in Cuba, all in people older than 15 years, after an infection with DENV-2 serotype. All but three cases were shown to have been previously infected by DENV-1 virus, during the epidemic of 1977–1979.[4] Two outbreaks of the disease occurred after the first epidemic in 1977-1979, one in 1981 and one in 1997. People who had been infected with DENV-1 during the 1977-79 outbreak and secondarily infected with DENV-2 in 1997 had 3 to 4 more chances to develop a severe disease than those secondarily infected with DENV-2 in 1981.[5] While heterotypic antibody titers decrease, homotypic antibody titers increase during long time periods (4 to 20 years). This could be due to the preferential survival of long-lived B memory cells producing homotypic antibodies, thanks to their bigger affinity [5].This cross-reactive protection does not persist more than 3 months. The decrease of cross-reactive neutralizing antibodies titers in the serum could be the reason for more severe secondarily infections. Moreover, infection with DENV induces cross-reactive but weak- or non-neutralizing antibodies.[6]


There are several possibilities to explain the phenomenon:

  1. A viral surface protein laced with antibodies against a virus of one serotype binds to a similar virus with a different serotype. The binding is meant to neutralize the virus surface protein from attaching to the cell, but the antibody bound to virus also binds to the receptor of the cell, the Fc-region antibody receptor FcγR. This brings the virus into close proximity to the virus-specific receptor, and the cell endocytoses the virus through the normal infection route.[7]
  2. A virus surface protein may be attached to antibodies of a different serotype, activating the classical pathway of the complement system. The complement cascade system instead binds C1q attached to the virus surface protein via the antibodies, which in turn bind C1q receptor found on cells, bringing the virus and the cell close enough for a specific virus receptor to bind the virus, beginning infection.. This mechanism as not been shown specifically for the dengue virus infection, but is supposed to occur with Ebola virus infection in vitro.[8]
  3. When an antibody to a virus is present for a different serotype, it is unable to neutralize the virus, which is then ingested into the cell as a sub-neutralized virus particle. These viruses are phagocytosed as antigen-antibody complexes, and degraded by macrophages. Upon ingestion the antibodies no longer even sub-neutralize the body due to the denaturing condition at the step for acidification of phagosome before fusion with lysosome. The virus becomes active and begins its proliferation within the cell.


  1. ^ Boonnak K, Slike BM, Burgess TH, et al. (April 2008). "Role of dendritic cells in antibody-dependent enhancement of dengue virus infection". Journal of Virology 82 (8): 3939–51. doi:10.1128/JVI.02484-07. PMID 18272578.  
  2. ^ a b King CA, Anderson R, Marshall JS (August 2002). "Dengue virus selectively induces human mast cell chemokine production". Journal of Virology 76 (16): 8408–19. PMID 12134044. PMC 155122.  
  3. ^ a b Alvarez G, Piñeros JG, Tobón A, et al. (October 2006). "Efficacy of three chloroquine-primaquine regimens for treatment of Plasmodium vivax malaria in Colombia". The American Journal of Tropical Medicine and Hygiene 75 (4): 605–9. PMID 17038680.  
  4. ^ . doi:10.1093/aje/152.9.804.  
  5. ^ a b Guzman MG, Alvarez M, Rodriguez-Roche R, et al. (February 2007). "Neutralizing antibodies after infection with dengue 1 virus". Emerging Infectious Diseases 13 (2): 282–6. PMID 17479892. PMC 2725871.  
  6. ^ Goncalvez AP, Engle RE, St Claire M, Purcell RH, Lai CJ (May 2007). "Monoclonal antibody-mediated enhancement of dengue virus infection in vitro and in vivo and strategies for prevention". Proceedings of the National Academy of Sciences of the United States of America 104 (22): 9422–7. doi:10.1073/pnas.0703498104. PMID 17517625.  
  7. ^ Takada A, Kawaoka Y (2003). "Antibody-dependent enhancement of viral infection: molecular mechanisms and in vivo implications". Reviews in Medical Virology 13 (6): 387–98. doi:10.1002/rmv.405. PMID 14625886.  
  8. ^ Takada A, Feldmann H, Ksiazek TG, Kawaoka Y (July 2003). "Antibody-dependent enhancement of Ebola virus infection". Journal of Virology 77 (13): 7539–44. PMID 12805454. PMC 164833.  


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