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

Abstract

BackgroundRecently 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.ResultsAfter 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.ConclusionsOur 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.

Low CD4/CD8 ratio in classical swine fever postnatal persistent infection generated at 3 weeks after birth

“…Consequently, considering the low CD4/CD8 ratio and the reduced impact of the cytokine storm phenomenon, at least in terms of IFN-α, evidenced in CSFV persistently infected animals after super-infection with CSFV or African swine fever virus (Cabezón et al, 2017;Muñoz-González et al, 2016); we suggest the possible implication of the immune exhaustion mechanism that may favour the constant and high CSFV replication levels during CSFV persistence (Cabezón et al, 2017;Muñoz-González et al, 2016). Nevertheless, further studies will be performed to clarify the role of the immune exhaustion phenomenon and other immunosuppressive disorders in the CSFV pathogenesis.…”

Foetal Immune Response Activation and High Replication Rate during Generation of Classical Swine Fever Congenital Infection

“…Previous reports have shown that the levels of sCD163 can be increased as a result of tissue damage during acute infection with highly pathogenic viruses, such as the African swine fever virus (ASFV) [39,40]. In addition, increased IFN-γ levels have also been found as part of the cytokine storm phenomenon responsible for the pathogenesis of ASFV [39][40][41].…”

“…Previous reports have shown that the levels of sCD163 can be increased as a result of tissue damage during acute infection with highly pathogenic viruses, such as the African swine fever virus (ASFV) [39,40]. In addition, increased IFN-γ levels have also been found as part of the cytokine storm phenomenon responsible for the pathogenesis of ASFV [39][40][41]. In agreement with the haemorrhagic lesions and levels of viral replication found in foetuses infected with the high virulence CSFV Margarita strain, it is likely that the increase of IFN-γ and sCD163 may be associated with the exacerbated immune response in the host after infection, leading to cellular homeostasis imbalance and tissue damage.…”

“…Commercial ELISA test was used for detection of IFN-γ (IFN-γ ELISA Kit, Porcine, Life Technologies), following the manufacturer's instructions and the results were expressed as picograms per millilitre (pg/ml). Finally, a formerly described ELISA using lysates from CD163 transfected CHO cells as standard was used to quantify sCD163 [39,52]. Results were expressed as the equivalent numbers of CD163-transfected CHO cells (ENC).…”

African Swine Fever: Penyakit Emerging yang Mengancam Peternakan Babi di Dunia

“…Manifestasi infeksi ASF menghasilkan 4 bentuk gejala klinis seperti perakut, akut, subakut dan kronis, tergantung dari virulensi strain yang menginfeksi, strain babi dan status kekebalan (Sanchez-Vizcano et al 2015). Umumnya, babi liar seperti babi hutan lebih rentan terhadap infeksi ASF dan tidak menimbulkan gejala klinis yang khas, namun dapat bertindak sebagai karier virus ASF (Cabezón et al 2017).…”