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.