Chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus that has emerged in recent years as a major human pathogen. CHIKV causes major epidemics every year, mostly in Africa, Asia and the Americas. In recent years (2004-2015), CHIKV has caused the largest ever recorded alphavirus outbreak with an estimated 1.4 - 6.5 million cases across nearly 40 countries, with its latest spread to the Americas (>1 million cases).
Chikungunya means “disease that bends up the joints” in Tanzanian Makonde dialect, referring to the major manifestation of this disease. Chikungunya symptoms first become apparent 3-7 days after the bite from an infected mosquito. The major symptoms of acute CHIKV infection are fever, severe and debilitating joint and muscle pain, headache, joint swelling and rash. While serious complications are rare, fatal infections have been reported in the elderly and immunocompromised individuals. Probably the most significant consequence of CHIKV infection is the long-lasting joint manifestations—chronic arthralgia, fatigue and musculoskeletal injury—that can persist for months or even years. These long-term manifestations lead to considerable economic and social burden. There are currently no vaccines or specific drugs available to treat CHIKV infection.
Over the last decade, we have made considerable progress in understanding the biology of CHIKV and the underlying pathology of this disease. However, the contributions of innate and adaptive immunity to virus clearance and resolution of disease still remain unclear. CHIKV is especially sensitive to the antiviral activity of type I interferons. A number of viral factors have been implicated in this disease by, for example, modulating the antiviral activity of IFNs and other immune pathways such as inflammasomes and complement pathways. The host immune response plays a crucial role in controlling CHIKV infection. The heightened activity of macrophages, T cells and immune mediators such as cytokines, chemokines and complement proteins substantially contribute to the immunopathology of the disease. The recent discovery of the host cellular receptor for CHIKV is likely to lead to new insights into disease pathogenesis. While our understanding of the CHIKV-host interactions has increased dramatically over the last decade, several questions remain unanswered.
In this Research Topic, we welcome the submission of Original Research articles, Reviews, Clinical Trials and Case Reports that will broadly cover:
(i) Innate and adaptive immune responses to CHIKV infection.
(ii) Immunopathology and disease resolution of CHIKV infection.
(iii) Viral factors underlying the immunopathology in CHIKV infection.
(iv) Approaches to vaccine development against CHIKV infection.
(v) Experimental model systems to study CHIKV infection including in vitro studies with primary cells and studies in mouse and non-human primate models.
Chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus that has emerged in recent years as a major human pathogen. CHIKV causes major epidemics every year, mostly in Africa, Asia and the Americas. In recent years (2004-2015), CHIKV has caused the largest ever recorded alphavirus outbreak with an estimated 1.4 - 6.5 million cases across nearly 40 countries, with its latest spread to the Americas (>1 million cases).
Chikungunya means “disease that bends up the joints” in Tanzanian Makonde dialect, referring to the major manifestation of this disease. Chikungunya symptoms first become apparent 3-7 days after the bite from an infected mosquito. The major symptoms of acute CHIKV infection are fever, severe and debilitating joint and muscle pain, headache, joint swelling and rash. While serious complications are rare, fatal infections have been reported in the elderly and immunocompromised individuals. Probably the most significant consequence of CHIKV infection is the long-lasting joint manifestations—chronic arthralgia, fatigue and musculoskeletal injury—that can persist for months or even years. These long-term manifestations lead to considerable economic and social burden. There are currently no vaccines or specific drugs available to treat CHIKV infection.
Over the last decade, we have made considerable progress in understanding the biology of CHIKV and the underlying pathology of this disease. However, the contributions of innate and adaptive immunity to virus clearance and resolution of disease still remain unclear. CHIKV is especially sensitive to the antiviral activity of type I interferons. A number of viral factors have been implicated in this disease by, for example, modulating the antiviral activity of IFNs and other immune pathways such as inflammasomes and complement pathways. The host immune response plays a crucial role in controlling CHIKV infection. The heightened activity of macrophages, T cells and immune mediators such as cytokines, chemokines and complement proteins substantially contribute to the immunopathology of the disease. The recent discovery of the host cellular receptor for CHIKV is likely to lead to new insights into disease pathogenesis. While our understanding of the CHIKV-host interactions has increased dramatically over the last decade, several questions remain unanswered.
In this Research Topic, we welcome the submission of Original Research articles, Reviews, Clinical Trials and Case Reports that will broadly cover:
(i) Innate and adaptive immune responses to CHIKV infection.
(ii) Immunopathology and disease resolution of CHIKV infection.
(iii) Viral factors underlying the immunopathology in CHIKV infection.
(iv) Approaches to vaccine development against CHIKV infection.
(v) Experimental model systems to study CHIKV infection including in vitro studies with primary cells and studies in mouse and non-human primate models.
