Abstract
The tremendous global surging of the African Swine Fever Virus (ASFV)
threatens pig industries worldwide. ASFV causes acute hemorrhagic fever
in domestic pigs with near enough 100 % mortality, whereas immune in
its natural host’s warthogs, bush-pigs, and the soft tick vector. ASFV
is a large cytoplasmic double-stranded DNA virus that replicates mainly
in macrophages. At present, infected animals can only be managed by
quarantine and removal of infected animals as lack of effective vaccines
and treatment. This review focus on mechanisms by which ASFV enter,
replicate, modulate, molecular hijacking and overpowered the host immune
system. Various machinery employed by ASFV discussed, such as overcoming
barriers to replication in the monocyte/macrophage, inhibition of
apoptosis, inhibition of inflammatory responses, ASFV adhesion protein
CD2v. This review exposes ASFV evasion strategies and virus-host
interactions, thus reveal promising vaccine development ideas.
Introduction to African Swine Fever Virus (ASFV)
African Swine Fever (ASF) is a highly contagious and deadly haemorrhage
disease of swine with extensive virulence in morbidity and high
mortality rates that approach 100% (Gallardo et al., 2015). Currently,
vaccines and treatments are not available; the disease can only be
managed by quarantine and removing infected animals. This disease is
endemic in sub-Sahara Africa, Asia, and Europe, which affects the pork
industry in those regions and also causes socio-economic losses
worldwide (Costard et al., 2009). The diseases are characterized by high
fever, haemorrhages, ataxia, bleeding, and depression in swine.
A large double-stranded DNA virus causes ASF with a complex molecular
structure. African Swine Fever Virus (ASFV) is a cytoplasmic replicated
virus that belongs to the superfamily of nucleocytoplasmic large DNA
viruses (NCLDV) (Dixon et al., 2005, 2008; Iyer et al., 2006; Yutin et
al., 2009). African Swine Fever Virus belongs to a member of the
Asfarviridae family, genus Asfivirus (Dixon et al., 2008). In Africa,
Ornithodoros species like warthogs, bushpigs, and soft ticks are the
virus long-term reservoir hosts without significant clinical signs. ASFV
has icosahedral morphology with an average diameter of 200nm. The genome
consists of nucleoids wrapped by a protein core-shell, an inner lipid
membrane, protein capsid, and other membranes. ASFV genome contains
double-stranded DNA of 170-194kbp single linear molecule, covalently
close-ended.
Understanding the mechanisms ASFV uses to invade and modulates host
defense responses to infection will buttress strategies and knowledge
accurately needed for vaccine development.
ASFV DNA genome encodes many proteins; about 160 non-essential of the
said proteins have no value for virus replication but play essential
roles in evading and modulating host defences response. ASFV codes for
many proteins which inhibit interferon responses, antiviral response.
The virus target replication cells are the mononuclear phagocyte system
having critical roles in activating innate and adaptive responses.
Therefore, ASFV rendering these cells incapacitated by profoundly
manipulating their functions in response to infections (Dixon et al.,
2019).
An essential feature of host defence, operating immediately upon
infection with these viruses, is a cell’s capacity to induce intrinsic
and innate immune responses against DNA viruses. These host defences
function to prevent viral infection as well as to support the adaptive
immune responses within the host organism and to promote a global
antiviral environment. As such, for the survival of the host and the
preservation of a balanced system, these immune processes’ role is
essential. Immune system misregulation is associated with the
progression of debilitating autoimmune disorders, including type I
diabetes, multiple sclerosis, and erythematosus lupus (reviewed in Lang
et al., 2007).
In this review, mechanisms by which ASFV invade and manipulate host
defences system were described, such as overcoming barriers to
replication in the monocyte/macrophage, inhibition of apoptosis,
inhibition of inflammatory responses, ASFV adhesion protein CD2v.