Phylodynamics and evolutionary epidemiology of African swine fever p72-CVR genes in Eurasia and Africa

Abstract

African swine fever (ASF) is a complex infectious disease of swine that constitutes devastating impacts on animal health and the world economy. Here, we investigated the evolutionary epidemiology of ASF virus (ASFV) in Eurasia and Africa using the concatenated gene sequences of the viral protein 72 and the central variable region of isolates collected between 1960 and 2015. We used Bayesian phylodynamic models to reconstruct the evolutionary history of the virus, to identify virus population demographics and to quantify dispersal patterns between host species. Results suggest that ASFV exhibited a significantly high evolutionary rate and population growth through time since its divergence in the 18th century from East Africa, with no signs of decline till recent years. This increase corresponds to the growing pig trade activities between continents during the 19th century, and may be attributed to an evolutionary drift that resulted from either continuous circulation or maintenance of the virus within Africa and Eurasia. Furthermore, results implicate wild suids as the ancestral host species (root state posterior probability = 0.87) for ASFV in the early 1700s in Africa. Moreover, results indicate the transmission cycle between wild suids and pigs is an important cycle for ASFV spread and maintenance in pig populations, while ticks are an important natural reservoir that can facilitate ASFV spread and maintenance in wild swine populations. We illustrated the prospects of phylodynamic methods in improving risk-based surveillance, support of effective animal health policies, and epidemic preparedness in countries at high risk of ASFV incursion.

Re‐emergence of genotype I of African swine fever virus in Ivory Coast

“…The CVR analysis revealed two types of profiles which are very close to those of isolates from Cameroon (Alkhamis et al., ). p72 analysis combined with the p54 and CVR characterization has been shown to be an effective approach for determining a relationship between ASF outbreaks and to determine the possible sources of infection (Gallardo et al., ; Penrith et al., ).…”

“…The CVR analysis revealed two distinct tetrameric repeat amino acid signatures (Table ) differing by an insertion A (CAST). Isolates (IC‐SP/2014/3 and IC‐SP/2014/1 from San‐Pedro shared common CVR profiles with isolates Cam10/YGT9; Cam10/GGT5, Cam10/OGT13 collected in 2010 in Cameroon (Alkhamis et al., ). All isolates from Moussadougou and the remaining isolates from San‐Pedro shared common CVR profiles with isolates CAM/1/86 () and CAM/82 () collected in 1986 and 1982 in Cameroon.…”

“… The CVR sequences of additional 50 ASFV of genotype I from Western and Central Africa as well as Angola where retrieved from Genbank (15) or the supplement file of the paper by Alkhamis et al. () and compared with 2014 ASFVs from Ivory Coast. …”

“…ASVF genotype I sequences from neighbouring countries (Benin, Burkina, Ghana, and Togo) as well as those from countries whose boats visited the seaport of San‐Pedro around the outbreak period (Ghana, Angola and Cameroon) were included as well. Up to 62 sequences of ASFV collected from Angola, Cameroon, Ghana, Benin, Togo, Nigeria and Burkina Faso between 2015 and 2010 were initially collected: 31 were from Genbank and 31 other were from the supplement material of a paper by Alkhamis et al., . However, the sequence alignment showed that all were 100% identical to the partial p72 gene sequence of isolate Ang72 (), therefore, only 12 were kept in the final data set for this study.…”

“…were from Genbank and 31 other were from the supplement material of a paper by Alkhamis et al, 2018. However, the sequence alignment showed that all were 100% identical to the partial p72 gene sequence of isolate Ang72 (FJ174378), therefore, only 12 were kept in the final data set for this study.…”