BACKGROUND AND RATIONALE OF THE CURRENT STUDY

Chikungunya virus (CHIKV) is an arthritic old world alphavirus transmitted mainly by Aedes species of mosquitoes [1, 2]. Its genome is composed of a single molecule of 11.8 kb positive sense single strand RNA which encodes two polyproteins i.e. non-structural and structural. The nonstructural polyprotein is cleaved into four mature non-structural proteins (nsP 1-4) by the viral protease nsP2 while the structural polyprotein produces five structural proteins (Capsid, E3, E2, 6k and E1). The febrile illness caused by this virus among humans is characterised by a triad of symptoms involving high fever, rash and chronic arthralgia [3]. Chikungunya disease gets its name from Kimakonde vernacular language which means “that contorts or bends up ” [4, 5]. CHIKV was first isolated in 1952 from the Makonde plateau in Tanzania, and since then has been responsible for a number of massive epidemic outbreaks posing major public health issues throughout the world. Although this virus is listed by National Institute of Allergy and Infectious diseases (NIAID) as a Priority C pathogen, that has been spreading throughout Asia, Africa and parts of Europe [6-8], there has been no commercially available vaccine or antiviral for this virus. The mechanism of infection and pathogenesis of CHIKV are poorly understoo