As Chikungunya virus is spreading by mosquitoes and causes severe joint and muscle pain. Approximately 30 to 60% of people infected with the virus continue to experience joint pain for months to years after the initial infection. However, the cause of this persistent joint pain is unclear, as replicating virus cannot be detected during the chronic phase.
To address this question, researchers developing a reporter system to permanently mark cells infected by chikungunya virus. A new method for permanently marking cells infected with chikungunya virus could reveal how the virus continues to cause joint pain for months to years after the initial infection. According to the authors, uncovering the mechanisms for long-term disease could aid in the development of treatments and preventative measures for this incapacitating, virally induced chronic arthritis.
The Chikungunya virus
Using this system, they show in mice that marked cells surviving chikungunya virus infection are a mixture of muscle and skin cells that are present for at least 112 days after initial virus inoculation. Treatment of mice with an antibody that blocks chikungunya virus infection reduces the number of marked cells in the muscle and skin. Moreover, surviving marked cells contain most of the persistent chikungunya virus RNA.
Taken together, the findings provide further evidence for musculoskeletal cells; as targets of chikungunya virus infection in the acute and chronic stages of disease. According to the authors, this reporter system represents a useful tool for identifying; and isolating cells that harbor chronic viral RNA in order to study the mechanisms underlying chronic disease.
But this persistent CHIKV RNA can be detected in human; and animal models but no one has been able to identify where the RNA resides due to insensitive techniques; Using our reporter system we have demonstrated that cells can survive CHIKV infection; and these cells harbor most of the persistent RNA. Since many believe that this persistent RNA contributes to chronic arthritis; this system will be a useful tool to study the mechanisms underlying chronic disease.
In conclusion, our CHIKV-3ʹ-Cre and tdTomato system provides further evidence for musculoskeletal cells; as targets of CHIKV infection in the acute and chronic stages of disease and revealing that fibroblasts; that survive acute CHIKV harbor persistent CHIKV RNA. How these cells contribute to pathogenesis remains to be elucidated. Uncovering the mechanisms for long-term pathogenesis could aid in the development of treatments and preventative measures for this incapacitating; virally-induced chronic arthritis.