Key result
Coxsackievirus B4 can infect, replicate, and persist in M-CSF-induced monocyte-derived macrophages, but not in GM-CSF-induced macrophages, while inducing high levels of IL-6 and TNFα.
CVB4 can replicate and persist in M-CSF-induced human monocyte-derived macrophages, suggesting a potential mechanism for viral persistence in chronic diseases.
May implicate M-CSF macrophages in CVB4 persistence; leaves open human chronic disease relevance.
Beyond acute infections, group B coxsackieviruses (CVB) are also reported to play a role in the development of chronic diseases, like type 1 diabetes. The viral pathogenesis mainly relies on the interplay between the viruses and innate immune response in genetically-susceptible individuals. We investigated the interaction between CVB4 and macrophages considered as major players in immune response. Monocyte-derived macrophages (MDM) generated with either M-CSF or GM-CSF were inoculated with CVB4, and infection, inflammation, viral replication and persistence were assessed. M-CSF-induced MDM, but not GM-CSF-induced MDM, can be infected by CVB4. In addition, enhancing serum was not needed to infect MDM in contrast with parental monocytes. The expression of viral receptor (CAR) mRNA was similar in both M-CSF and GM-CSF MDM. CVB4 induced high levels of pro-inflammatory cytokines (IL-6 and TNFα) in both MDM populations. CVB4 effectively replicated and persisted in M-CSF MDM, but IFNα was produced in the early phase of infection only. Our results demonstrate that CVB4 can replicate and persist in MDM. Further investigations are required to determine whether the interaction between the virus and MDM plays a role in the pathogenesis of CVB-induced chronic diseases.
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Alidjinou et al. (2015) studied Coxsackievirus B4 infection. Coxsackievirus B4 (CVB4) inoculation vs. GM-CSF-induced macrophages was evaluated on Infection, inflammation, viral replication and persistence. Coxsackievirus B4 can infect, replicate, and persist in M-CSF-induced monocyte-derived macrophages, but not in GM-CSF-induced macrophages, while inducing high levels of IL-6 and TNFα.
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