The 2005-2006 outbreak of chikungunya virus in the India Ocean Island left scientist wondering how this virus was able to re-emerge after going dormant. This epidemic caused several deaths among people infected with chikungunya virus. Scientist began to question the strategies and strains that might have enable CHIKV to thrive and cause this epidemic. They sought answers through understanding the replication cycle of the virus, its interaction with host’s cells as well as its genetic evolution. They also looked at how its genome is structured which would enable them to come up with ways to inhibit viral protein synthesis. Tsetsarkin et al. [1, 2] found that alanine was mutated to valine which resulted in a new chikungunya virus strain. Consequently, disease progression became very prevalent as 1/3 of 785,000 French island inhabitants got infected with chikungunya virus with 250 casualties reported. Chikungunya virus is single stranded having an RNA genome with two open reading frames encoding both nonstructural and structural viral proteins respectively. Chikungunya virus has envelope proteins (E1 and E2) which enhance initial binding of viral proteins to susceptible host’s cells. Their results showed that harringtonine (an antiviral) suppresses viral protein expression. It does this in the early stage of viral replication of CHIKV [2].
Figure1: showing viral replication of CHIKV
[1] Tsetsarkin, Konstantin A., et al. “A single mutation in chikungunya virus affects vector specificity and epidemic potential.” PLoS pathogens 3.12 (2007): e201.
[2] Kaur, Parveen, et al. “Inhibition of chikungunya virus replication by harringtonine, a novel antiviral that suppresses viral protein expression.” Antimicrobial agents and chemotherapy 57.1 (2013): 155-167.
Microbiology orange group 