Open veterinary journal · 2022
Inhibition of African swine fever virus replication by β-glucan.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tran Ha Thi Thanh, Truong Anh Duc, Chu Nhu Thi, Vu Hoai Nam, Nguyen Huyen Thi, Nguyen Tinh, Siti Fatimah, Lee Hans, Leon Alexander De, Yersin Andrew G, Dang Hoang Vu
Аннотация
BACKGROUND: African swine fever (ASF) is one of the most important diseases in pigs because of its effects on all ages and breeds. To date, commercial vaccines and drugs for the prevention of ASF are lacking in the market and the survival of African swine fever virus (ASFV) in various environmental, farm, and or feed matrices has allowed the virus to remain, causing new outbreaks in the pig population. Besides biosecurity and animal husbandry management practices, the improvement of the host immune responses is critical to control, managing, and preventing ASF.
AIM: In this study, we investigated the protective role of β-glucan against ASFV infection using a porcine alveolar macrophage (PAM) model.
METHODS: The effects of β-glucan on cell proliferation were evaluated by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The potential effects of β-glucan against a field ASFV strain isolated in Vietnam were further examined by real-time PCR and hemadsorption assays. The interferon (IFN)-α and interleukin (IL)-6 protein production induced by β-glucan was determined using a sandwich enzyme-linked immunosorbent assay.
RESULTS: Our results demonstrated that the β-glucan additive possessed an immune stimulus factor against ASFV. Specifically, protection of PAMs against ASFV infection in vitro was observed at 12 hours (p < 0.05) at the tested doses (30 and 50 µg/ml) as induced by incubation with β-glucan for 2 hours. These effects remained until 24 hours after post-infection. Additionally, at a high dose (50 µg/ml), pre-treatment with the β-glucan statistically increased the expression levels of IFNα and IL-6 when compared to untreated groups or only ASFV infection.
CONCLUSION: Together, these findings indicated that the β-glucan may protect the host against ASFV infection via the multiple cellular immune mechanisms.
AIM: In this study, we investigated the protective role of β-glucan against ASFV infection using a porcine alveolar macrophage (PAM) model.
METHODS: The effects of β-glucan on cell proliferation were evaluated by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The potential effects of β-glucan against a field ASFV strain isolated in Vietnam were further examined by real-time PCR and hemadsorption assays. The interferon (IFN)-α and interleukin (IL)-6 protein production induced by β-glucan was determined using a sandwich enzyme-linked immunosorbent assay.
RESULTS: Our results demonstrated that the β-glucan additive possessed an immune stimulus factor against ASFV. Specifically, protection of PAMs against ASFV infection in vitro was observed at 12 hours (p < 0.05) at the tested doses (30 and 50 µg/ml) as induced by incubation with β-glucan for 2 hours. These effects remained until 24 hours after post-infection. Additionally, at a high dose (50 µg/ml), pre-treatment with the β-glucan statistically increased the expression levels of IFNα and IL-6 when compared to untreated groups or only ASFV infection.
CONCLUSION: Together, these findings indicated that the β-glucan may protect the host against ASFV infection via the multiple cellular immune mechanisms.