Acquired immune deficiency syndrome (AIDS) caused by HIV is a serious threat to global public health . Despite intensive research since the 1980s there are no vaccines or drugs that can successfully prevent or eradicate the disease. The major barriers to HIV vaccine development include the variability of HIV, lack of a suitable ani mal model , lack of correlates of protective immunity , lack of natural protective immune response s against HIV, and the reservoir of infected cells conferred by integration of HIV’s genome into the host [ 1 ]. Within the main HIV-1 subgroup, Group M, there are nine clades as well as dozens of recombinant forms, and clades can vary up to 42 % at the amino acid level [ 2 ]. A vaccine immunogen derived from a particular clade may therefore be ineffective against other clades, posing a significant obstacle to the creation of a global HIV vaccine. Importantly, one of the principal barriers limiting discovery of an HIV vaccine has been that protective immune response s tend to be polyclonal and involve antibodies directed to several different epitopes; thus, antigenic variation among the different HIV-1 isolates has been the major problem in the development of an effective vaccine against AIDS [ 1 ]. Although several 3D structures of HIV-1 envelope protein fragments have been determined, this knowledge has not yet led to the design of an HIV-1 vaccine. The mechanism by which an HIV vaccine might confer protection therefore remains uncertain, and an effective vaccine may require induction of an immune response that is significantly different from that seen during natural infection [ 3 ]. Overall, current vaccination strategies have not helped in developing a vaccine for HIV; hence novel “out-of-the-box” strategies are essential in developing an HIV vaccine [ 4 ].

Ebola virus disease is a severe, often fatal, zoonotic infection caused by a virus of the Filoviridae family. The Ebola virus (EBOV) causes an acute viral syndrome that presents with fever and an ensuing bleeding diathesis that is marked by high mortality in human and nonhuman primate s. Fatality rates are higher than other viral diseases with rates of up to 90 % [ 5 ]. Ebola viral disease (EVD) affects the poorest people in the African continent. Due to movement of people across borders the disease could rapidly spread and infect any people globally. EBOV spreads through human-to- human transmission via direct contact with the blood, secretions, organs, or other bodily fluids of infected people and with surfaces and materials (e.g., bedding, clothing) contaminated with these fluids. EBOV glycoprotein (GP1,2) and matrix protein (VP40) are both major components of EBOV. The hemorrhagic disease caused by EBOV is characterized by generalized fluid distribution problems, hypotension, coagulation disorders, and a tendency to bleed, finally resulting in fulminant shock. Vascular instability and dysregulation are hallmarks of the pathogenesis in EBOV hemorrhagic fever (HF). Endothelial disturbances can be caused indirectly, by proinflammatory cytokines such as TNF-α released from EBOV-infected monocytes/macrophages, and directly, following virus infection of endothelial cells. In vitro studies demonstrated that EBOV viral proteins could activate endothelial cells and induce a decrease in blood vessel barrier function [ 6 ]. The worldwide challenge posed by the 2014 outbreak of EBOV [ 7 ] has underscored the need for effective prevention and treatment options, especially for front-line health care and emergency response workers in the fi eld, and at hospitals and other care facilities. As yet there are no vaccines or therapeutics commercially available to protect against EVD. Hence, there is an urgent need to develop a powerful vaccine which could provide robust protection against the viral pathogen . The EBOV and its high fatality are known since the 1970s. The disease only affects a small percentage of people annually in Africa; hence government agencies as well as International Organizations were not keen to invest in vaccines. If there were vaccines available against EBOV infection, thousands of lives could have been saved in 2014.

References
--------------

[1] Thomas S, Luxon BA (2013) Vaccines based on structure-based design provide protection against infectious diseases. Expert Rev Vaccines 12:1301–1311

[2] Hemelaar J (2012) The origin and diversity of the HIV-1 pandemic. Trends Mol Med 18:182–192

[3] Johnston M, Fauci A (2011) HIV vaccine development—improving on natural immunity. N Engl J Med 365:873–875

[4] Cohen YZ, Dolin R (2013) Novel HIV vaccine strategies: overview and perspective. Ther Adv Vaccines 1:99–112

 [5] Hoenen T, Groseth A, Feldmann H (2012) Current ebola vaccines. Expert Opin Biol Ther 12:859–872

[6] Wahl-Jensen VM, Afanasieva TA, Seebach J, Ströher U et al (2005) Effects of Ebola virus glycoproteins on endothelial cell activation and barrier function. J Virol 79: 10442–10450

[7] Weyer J, Grobbelaar A, Blumberg L (2015) Ebola virus disease: history, epidemiology and outbreaks. Curr Infect Dis Rep 17:480