Anti-Classical Swine Fever Virus Strategies

Abstract

Classical swine fever (CSF), caused by CSF virus (CSFV), is a highly contagious swine disease with high morbidity and mortality, which has caused significant economic losses to the pig industry worldwide. Biosecurity measures and vaccination are the main methods for prevention and control of CSF since no specific drug is available for the effective treatment of CSF. Although a series of biosecurity and vaccination strategies have been developed to curb the outbreak events, it is still difficult to eliminate CSF in CSF-endemic and re-emerging areas. Thus, in addition to implementing enhanced biosecurity measures and exploring more effective CSF vaccines, other strategies are also needed for effectively controlling CSF. Currently, more and more research about anti-CSFV strategies was carried out by scientists, because of the great prospects and value of anti-CSFV strategies in the prevention and control of CSF. Additionally, studies on anti-CSFV strategies could be used as a reference for other viruses in the Flaviviridae family, such as hepatitis C virus, dengue virus, and Zika virus. In this review, we aim to summarize the research on anti-CSFV strategies. In detail, host proteins affecting CSFV replication, drug candidates with anti-CSFV effects, and RNA interference (RNAi) targeting CSFV viral genes were mentioned and the possible mechanisms related to anti-CSFV effects were also summarized.

PCBP1 Deficient Pigs Hold the Potential to Inhibit CSFV Infection

“…CSFV, the pathogen of CSF which is characterized by multiple hemorrhages, leukopenia, high fever, abortion, and neurological dysfunction [1, 24] , has caused significant economic losses worldwide. Production of transgenic pigs is one of the powerfully effective strategies to contain viral infection by alteration of immune state genetically which has been widely utilized to resist various porcine viruses [25-28] .…”

“…Classical swine fever (CSF), driven by CSF virus (CSFV), is a highly contagious porcine disease, causing substantial economic losses [1, 2] and the typical clinical signs are generally characterized by high fever, inappetence, and general weakness followed by neurological deterioration, skin hemorrhages, and splenic infarction [3, 4] . The genome of CSFV could encode four structure proteins (C, E rns , E1, and E2) and eight non-structure proteins (N pro , p7, NS3, NS4A, NS4B, NS5A, and NS5B), which would utilize host factors for enhancing replication and evading cellular immunity [5] .…”

Transboundary Animal Diseases, an Overview of 17 Diseases with Potential for Global Spread and Serious Consequences

“…As with African swine fever, following strict biosecurity practices is imperative. Control of movement, adequate surveillance, and prophylactic and emergency vaccination are potentially useful in successful eradication and control programs [194,[226][227][228][229]. Also, as in African swine fever, additional consideration must be given to the presence of infected wild boar [230][231][232][233][234][235].…”

Cellular ESCRT components are recruited to regulate the endocytic trafficking and RNA replication compartment assembly during classical swine fever virus infection

“…The uncapped 5 0 -UTR carries an internal ribosome entry site (IRES), and the 3 0 -UTR is uridine-rich. The ORF encodes a polyprotein that is cleaved into four structural (capsid protein C, envelope glycoproteins Erns, E1, and E2) and eight nonstructural proteins (Npro, p7, NS2, NS3, NS4A, NS4B, NS5A and NS5B) [19,20]. Though cell entry is the critical step in the virus replication cycle, the host receptor of CSFV has not been identified.…”