The first vaccine against Dengue could be in the offing. Scientists have drawn the structure of the human antibody which will fight this deadly virus. Researchers affiliated with the Vanderbilt University and the National University of Singapore has unraveled the structure of the human monoclonal antibody. The antibody in an animal model effectively neutralizes a potentially virulent dengue virus.
Dengue is a complex of four distinct but mosquito-borne virus. The deciphering of the monoclonal antibody that effectively kills the lethal dengue could lead to effective therapies and vaccines against all the four forms of Dengue. Dengue infects about 390 million people every year and has been indicted as the major cause of illness and death in the tropics.
Co-corresponding author James Crowe Jr revealed the importance of the antibody discovery by the Vanderbilt Vaccine Centre which has carved a niche in perfecting antiviral drugs, such as the human antibody that not only destroys dengue virus but also preempts enhanced dengue disease.
The four separate or “serotypes” versions of the Dengue virus are proteins on the outer viral wall that elicits the immune response by the body. Dengue is a tricky virus because antibodies that are generated against one serotype will not protect against the others. In fact, such a scenario is even more dangerous because it could enhance infection by a second serotype in a condition termed as antibody-dependent enhancement (ADE) of infection.
Scientists had earlier developed human monoclonal antibodies to fight a complex epitope that is the antigenic section of the viral cover. The latest study involves freezing the samples to extremely low temperatures that enable the scientists to observe the antibody –antigen binding almost to the atomic level.
Researchers could identify human monoclonal antibody against dengue virus type 2 which bonded across an array of outer cover proteins. In mouse, this stopped the virus from fusing with its target cell thus preventing the infection. The antibody also served a second function; it also prevents the binding of other class of antibodies which would have augmented the infection.
The research was published in the journal Science.