African swine fever virus infection in Classical swine fever subclinically infected wild boars.

African swine fever virus infection in Classical swine fever subclinically infected wild boars.
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DOI:
10.1186/s12917-017-1150-0
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发表时间:
2017-08-01
影响因子:
2.6
通讯作者:
Ganges L
Ganges L
中科院分区:
农林科学2区
文献类型:
--
作者:
Cabezón O;Muñoz-González S;Colom-Cadena A;Pérez-Simó M;Rosell R;Lavín S;Marco I;Fraile L;de la Riva PM;Rodríguez F;Domínguez J;Ganges L

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近年来,中等毒力的猪瘟病毒(CSFV)毒株已被证明能够产生出生后持续感染(PI),定义为维持病毒血症和不能在动物中产生CSFV特异性免疫应答。这些动物在没有临床体征的情况下也显示I型干扰素阻断。在这项研究中,我们评估了非洲猪瘟病毒(ASFV)感染7周龄CSFV PI野猪后产生的感染。将感染ASFV的野猪分为两组。A组包括亚临床形式的CSFV PI的公猪,B组包括无瘟病毒的野猪。研究了与猪瘟病毒复制有关的一些参数和猪瘟病毒感染动物的免疫应答。此外,分析ASFV感染前后血清可溶性因子如IFN-α、TNF-α、IL-6、IL-10、IFN-γ和sCD 163,以评估它们在疾病进展中的作用。在ASFV感染后,只有CSFV PI野猪表现出进行性急性出血性疾病;然而,ASFV感染后的存活率在两个实验组中相似。尽管如此,CSFV PI动物的CSFV RNA载量在研究期间保持不变;同样,感染后检测到的ASFV DNA载量在组间相似。有趣的是,CSFV PI动物血清中全身I型FN-α和IL-10水平几乎检测不到,但在B组中可检测到,而在两组中均发现可检测水平的IFN-γ。最后,流式细胞术分析显示ASFV感染后来自CSFV P1动物的PBMC中的骨髓单核细胞(CD 172 a+)增加和CD 4 + T细胞减少。我们的研究结果表明,免疫反应在猪瘟病毒亚临床感染野猪ASFV感染后的疾病进展中起作用,免疫反应包括系统性I型干扰素阻断。ASFV不干扰CSFV的复制,反之亦然。ASFV感染可能是CSFV PI动物疾病进展的触发因素,因为它们在ASFV后的存活率与无瘟病毒的ASFV感染组相似。这一事实表明CSFV PI动物即使对ASFV等病毒也具有高抗性;这可能意味着在流行国家对CSF控制有相关意义。不能排除在流行国家诊断为ASFV和CSFV合并感染的可能性,需要进行更深入的研究。
Recently moderate-virulence classical swine fever virus (CSFV) strains have been proven capable of generating postnatal persistent infection (PI), defined by the maintenance of viremia and the inability to generate CSFV-specific immune responses in animals. These animals also showed a type I interferon blockade in the absence of clinical signs. In this study, we assessed the infection generated in 7-week-old CSFV PI wild boars after infection with the African swine fever virus (ASFV). The wild boars were divided in two groups and were infected with ASFV. Group A comprised boars who were CSFV PI in a subclinical form and Group B comprised pestivirus-free wild boars. Some relevant parameters related to CSFV replication and the immune response of CSFV PI animals were studied. Additionally, serum soluble factors such as IFN-α, TNF-α, IL-6, IL-10, IFN-γ and sCD163 were analysed before and after ASFV infection to assess their role in disease progression. After ASFV infection, only the CSFV PI wild boars showed progressive acute haemorrhagic disease; however, the survival rates following ASFV infection was similar in both experimental groups. Notwithstanding, the CSFV RNA load of CSFV PI animals remained unaltered over the study; likewise, the ASFV DNA load detected after infection was similar between groups. Interestingly, systemic type I FN-α and IL-10 levels in sera were almost undetectable in CSFV PI animals, yet detectable in Group B, while detectable levels of IFN-γ were found in both groups. Finally, the flow cytometry analysis showed an increase in myelomonocytic cells (CD172a+) and a decrease in CD4+ T cells in the PBMCs from CSFV PI animals after ASFV infection. Our results showed that the immune response plays a role in the progression of disease in CSFV subclinically infected wild boars after ASFV infection, and the immune response comprised the systemic type I interferon blockade. ASFV does not produce any interference with CSFV replication, or vice versa. ASFV infection could be a trigger factor for the disease progression in CSFV PI animals, as their survival after ASFV was similar to that of the pestivirus-free ASFV-infected group. This fact suggests a high resistance in CSFV PI animals even against a virus like ASFV; this may mean that there are relevant implications for CSF control in endemic countries. The diagnosis of ASFV and CSFV co-infection in endemic countries cannot be ruled out and need to be studied in greater depth.
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