Blood Counts, Biochemical Parameters, Inflammatory, and Immune Responses in Pigs Infected Experimentally with the African Swine Fever Virus Isolate Pol18_28298_O111

Abstract

This study aimed to indicate the influence of infection caused by genotype II African swine fever virus (ASFV)–isolate Pol18_28298_O111, currently circulating in Poland, on blood counts, biochemical parameters, as well as inflammatory and immune responses. Blood and sera collected from 21 domestic pigs infected intranasally with different doses of virulent ASFV were analysed. The infection led to variable changes in blood counts depending on the stage of the disease with a tendency towards leukopenia and thrombocytopenia. The elevated C-reactive protein (CRP) concentrations and microscopic lesions in organs confirmed the development of the inflammation process, which also resulted in an increased level of biochemical markers such as: Aspartate transaminase (AST), creatine kinase (CK), creatinine, and urea. Antibodies could be detected from 9 to 18 days post infection (dpi). Two survivors presented the highest titer of antibodies (>5 log10/mL) with a simultaneous increase in the lymphocyte T (CD3+) percentage–revealed by flow cytometry. Results confirmed a progressive inflammatory process occurring during the ASFV infection, which may lead to multiple organs failure and death of the majority of affected animals.

ASF -survivors’ sera do not inhibit African swine fever virus replication in vitro

“…Our study does not exclude the role of anti-ASF antibodies in the productive immune response to ASFV in vivo , since all examined sera were collected from survivor animals. This and a previously published study ( 31 ) underline the importance of possible interactions between humoral and cellular immunity in protection against the disease.…”

“…All serum donors were considered potential ASF survivors. Different clinical symptoms but a constant and low virus load in the blood had been recorded in the selected pigs during animal experiments conducted previously ( 31 , 32 ). The evolution of the viraemia of survivor pigs is shown in Fig.…”

“… Evolution of viraemia during a previously conducted experiment showing the comparison between survivor pigs (coloured and hollow symbol) and selected pigs with acute or subacute form of ASF (black solid symbol) ( 31 ). Cq - quantification cycle; dpi – days post inoculation …”

“…The large ASFV genome (170 to 193 kbp) consists of double-stranded DNA that may encode more than 150 proteins ( 9 ). The virus enters the target cells (mainly monocytes and macrophages) via constitutive macropinocytosis and clathrin-mediated endocytosis pathway ( 15 , 25 ) and causes massive, devastating inflammation in the host ( 31 , 33 ). Moreover, the virus is equipped with genes responsible for evading the host’s immune response ( 8 ), which enhance its virulence.…”

Regulation and Evasion of Host Immune Response by African Swine Fever Virus

“…Previous studies showed that virulent ASFV infection could promote the release of acute-phase proteins in serum, including serum amyloid A (SAA) and C-reactive protein (CRP), and increase the expression of a number of inflammatory cytokines, such as IL-1α, IL-1β, IL-6, and TNF-α ( Sanchez-Cordon et al, 2007 ; Walczak et al, 2021 ). Similarly, Wang et al (2020) found that virulent SY18 ASFV infection induced a robust and sustained elevation of pro-inflammatory cytokines (such as TNF-α, IL-1β, IL-6, IL-18, RANTES, and IP-10) from 3 days post-infection (dpi) and a secondary drastic increase including TNF-α, IL-1β, IL-6, and IL-8 and IL-10 at the terminal phase of infection in domestic pigs.…”