Abstract
Modulation of the expression of chemokines and chemokine receptors in whole blood was compared following infection of pigs with high and low virulence isolates of African swine fever virus. Levels of mRNAs for CCL2, CCL3L1, CCL4, CXCL10, CCR1 and CCR5 were significantly increased in at least one time point following infection in two experiments and CCL5, CCR9 and CXCR4 mRNA were significantly increased in one of the experiments. The results showed that greatest fold increases in mRNAs for CXCL10 and CCL2 were observed following infection of pigs. CXCL10 mRNA was increased by up to 15 fold in infected compared to uninfected pigs. CXCL10 protein was also detected in serum from pigs infected with the high virulence Benin 97/1 isolate. Levels of CCL2 mRNA were increased in pigs infected with high virulence Benin 97/1 isolate compared to low virulence OURT88/3 isolate and this correlated with an increase of greater than 30 fold in levels of CCL2 protein detected in serum from pigs infected with this isolate. An increase in overall chemotaxis active compounds in defibrinated plasma samples from Benin 97/1 infected pigs was observed at 3 days post-infection (dpi) and a decrease by 7 dpi as measured by chemotaxis assay using normal pig leucocytes in vitro. Increased levels of CXCL10 may either contribute to the activation of lymphocyte priming toward the Th1 phenotype or induction of T lymphocyte apoptosis. Increased levels of CCL2, a chemoattractant for macrophages, may result in increased recruitment of monocytes from bone marrow thus increasing the pool of cells susceptible to infection.
Highlights
African swine fever virus (ASFV) is a large doublestranded DNA virus and is the only member of the Asfarviridae family
Infections of pigs with ASFV To investigate the modulation of the host chemokine response caused by ASFV, pigs were infected with ASFV isolates of low (OURT88/3) or high virulence (Benin 97/ 1 or Uganda 1965) and whole blood samples were collected at different days post-infection
In experiment 1 one group of 6 pigs was infected with the low virulence genotype I OURT88/3 isolate, a second group of 5 pigs was infected with genotype I high virulence Benin 97/1 isolate and a third group of 4 pigs was infected with genotype X high virulence Uganda 1965 isolate
Summary
African swine fever virus (ASFV) is a large doublestranded DNA virus and is the only member of the Asfarviridae family. The genome varies between 170 and 193 kbp and encodes 150 to 167 open reading frames. The virus has been established in a sylvatic cycle in East and southern Africa, involving warthogs and soft ticks of Ornithodoros species, for an extended period. In these hosts infection is inapparent and the virus can cause persistent infections. Most ASFV isolates cause an acute haemorrhagic fever, African swine fever (ASF), in domestic pigs and wild boar resulting in high mortality. ASFV is endemic or causes sporadic outbreaks of disease in most sub-Saharan countries in Africa [1,2]
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