Classical swine fever virus: the past, present and future

Tembusu virus (TMUV, genus Flavivirus, family Flaviviridae) was first isolated in 1955 from Culex tritaeniorhynchus mosquitoes in Kuala Lumpur, Malaysia. In April 2010, duck TMUV was first identified as the causative agent of egg-drop syndrome, characterized by a substantial decrease in egg laying and depression, growth retardation and neurological signs or death in infected egg-laying and breeder ducks, in the People’s Republic of China. Since 2010, duck TMUV has spread to most of the duck-producing regions in China, including many of the coastal provinces, neighbouring regions and certain Southeast Asia areas (i.e. Thailand and Malaysia). This review describes the current understanding of the genome characteristics, host range, transmission, epidemiology, phylogenetic and immune evasion of avian-origin TMUV and the innate immune response of the host.

An updated review of avian-origin Tembusu virus: a newly emerging avian Flavivirus.

Interferons (IFNs) play crucial roles in host defense against viral infections by inducing the expression of numerous IFN-stimulated genes (ISGs) that can activate host antiviral immunity. Interferon-inducible transmembrane proteins (IFITMs), a family of small transmembrane proteins, are critical ISG products. Compelling evidence has implicated that IFITMs can establish an innate immune state to eliminate pathogens efficiently. IFITM proteins can impede broad-spectrum viral infection through various mechanisms. It is generally believed that IFITMs can block the viral entry by suppressing viral membrane fusion. However, some findings indicated that IFITMs might also inhibit viral gene expression and viral protein synthesis and thereby impair viral replication. IFITMs may incorporate into virions during viral assembly and thus reduce the infectivity of nascent virions. The precise inhibitory mechanism of IFITMs on viral infection and replication still requires further exploration. In this review, we highlight the recent findings regarding critical roles of IFITMs in host-virus interaction. We also discuss the molecular mechanisms underlying their functions in antiviral responses.

/pdf/functional-involvement-of-interferon-inducible-transmembrane-59ryxxtq0d.pdf

Functional Involvement of Interferon-Inducible Transmembrane Proteins in Antiviral Immunity.

Mallard ducks are a natural host and reservoir of avian Influenza A viruses. While most influenza strains can replicate in mallards, the virus typically does not cause substantial disease in this host. Mallards are often resistant to disease caused by highly pathogenic avian influenza viruses, while the same strains can cause severe infection in humans, chickens, and even other species of ducks, resulting in systemic spread of the virus and even death. The differences in influenza detection and antiviral effectors responsible for limiting damage in the mallards are largely unknown. Domestic mallards have an early and robust innate response to infection that seems to limit replication and clear highly pathogenic strains. The regulation and timing of the response to influenza also seems to circumvent damage done by a prolonged or dysregulated immune response. Rapid initiation of innate immune responses depends on viral recognition by pattern recognition receptors (PRRs) expressed in tissues where the virus replicates. RIG-like receptors (RLRs), Toll-like receptors (TLRs), and Nod-like receptors (NLRs) are all important influenza sensors in mammals during infection. Ducks utilize many of the same PRRs to detect influenza, namely RIG-I, TLR7, and TLR3 and their downstream adaptors. Ducks also express many of the same signal transduction proteins including TBK1, TRIF, and TRAF3. Some antiviral effectors expressed downstream of these signaling pathways inhibit influenza replication in ducks. In this review, we summarize the recent advances in our understanding of influenza recognition and response through duck PRRs and their adaptors. We compare basal tissue expression and regulation of these signaling components in birds, to better understand what contributes to influenza resistance in the duck.

/pdf/pattern-recognition-receptor-signaling-and-innate-responses-3nv91f7hcd.pdf

Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens.

Electronic cigarettes (E-cigarettes, ECs) are electronic devices that heat a liquid – usually comprising propylene glycol and glycerol, with or without nicotine and flavors, stored in disposable or refillable cartridges or a reservoir – into an aerosol (vapor) for inhalation [1]. Since ECs appeared on the market in 2006 they have become increasingly popular, especially among young people [1, 2]. E-cigarettes are marketed as a safer and “healthier” alternative to traditional cigarettes, and it is suggested in the mass media that ECs help smokers to stop smoking long-term, or to help smokers unable to stop smoking entirely to reduce their tobacco cigarette consumption [3]. However, the number of never-smoking youth who use ECs with or without nicotine is dramatically increasing. ECs are new sources of the highly addictive substance nicotine, which has a proven harmful effect on health [4, 5]. And, the advertising of nicotine-free ECs with liquids of fruit and sweet flavors is particularly likely to encourage young people to start using the E-cigarette. The Forum of International Respiratory Societies also revealed that E-cigarette (EC)-smoking is a significant public health problem because EC-use simulate smoking behaviour and can be done in public places, which together with its alarmingly growing popularity may increase the social approval for smoking and nicotine addiction [6]. In addition to the possible harmful effects of nicotine per se, the other main health concerns about EC-usage is the potential for toxic aldehyde emissions, such as formaldehyde, acetaldehyde, propanal and acrolein, which are known to be formed following heating of the EC-liquid main components propylene glycol and glycerol, as thermal decomposition products [7, 8]. Other contaminants inhaled by an EC-smoker during a “vaporization” session can be o-methyl-benzaldehyde,

/pdf/the-underestimated-danger-of-e-cigarettes-also-in-the-1uj1n5lnih.pdf

The underestimated danger of E-cigarettes - also in the absence of nicotine

Avian Tembusu virus (ATMUV) is a highly pathogenic flavivirus that causes significant economic losses to the Chinese poultry industry. Our previous experiments demonstrated that ATMUV infection effectively triggered host innate immune response through MDA5 and TLR3-dependent signaling pathways. However, little information is available on the role of interferon-stimulated genes (ISGs) in defending against ATMUV infection. In this study, we found that ATMUV infection induced robust expression of type I and type III interferon (IFNs) in duck tissues. Furthermore, we observed that expression of interferon-inducible transmembrane proteins (IFITMs) was significantly upregulated in DEF and DF-1 cells after infection with ATMUV. Similar results were obtained from in vivo studies using ATMUV-infected ducklings. Importantly, we showed that knockdown of endogenous IFITM1 or IFITM3 by specific shRNA markedly enhanced ATMUV replication in DF-1 cells. However, disruption of IFITM2 expression had no obvious effect on the ATMUV replication. In addition, overexpression of chicken or duck IFITM1 and IFITM3 in DF-1 cells impaired the replication of ATMUV. Taken together, these results reveal that induced expression of avian IFITM1 and IFITM3 in response to ATMUV infection can effectively restrict the virus replication, and suggest that increasing IFITM proteins in host may be a useful strategy for control of ATMUV infection.

/pdf/avian-interferon-inducible-transmembrane-protein-family-31kft7c3t2.pdf

Avian Interferon-Inducible Transmembrane Protein Family Effectively Restricts Avian Tembusu Virus Infection.

Role of innate immunity in pathophysiology of classical swine fever virus infection.

Infection of goats with goatpox virus triggers host antiviral defense through activation of innate immune signaling.

Avian Tembusu virus (ATMUV) is a newly emerged flavivirus that belongs to the Ntaya virus group. ATMUV is a highly pathogenic virus causing significant economic loss to the Chinese poultry industry. However, little is known about the role of host innate immune mechanism in defending against ATMUV infection. In this study, we found that ATMUV infection significantly up-regulated the expression of type I and type III interferons (IFN) and some critical IFN-stimulated genes (ISG) in vivo and in vitro. This innate immune response was induced by genomic RNA of ATMUV. Furthermore, we observed that ATMUV infection triggered IFN response mainly through MDA5 and TLR3-dependent signaling pathways. Strikingly, shRNA-based disruption of IPS-1, IRF3 or IRF7 expression significantly reduced the production of IFN in the 293T cell model. Moreover, NF-κB was shown to be activated in both chicken and human cells during the ATMUV infection. Inhibition of NF-κB signaling also resulted in a clear decrease in expression of IFN. Importantly, experiments revealed that treatment with IFN significantly impaired ATMUV replication in the chicken cell. Consistently, type I IFN also exhibited promising antiviral activity against ATMUV replication in the human cell. Together, these data indicate that ATMUV infection triggers host innate immune response through MDA5 and TLR3-dependent signaling that controls IFN production, and thereby induces an effective antiviral immunity.

/pdf/avian-tembusu-virus-infection-effectively-triggers-host-2x6n49ja03.pdf

Avian Tembusu virus infection effectively triggers host innate immune response through MDA5 and TLR3-dependent signaling pathways.

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Papers

Avian Interferon-Inducible Transmembrane Protein Family Effectively Restricts Avian Tembusu Virus Infection.

Role of innate immunity in pathophysiology of classical swine fever virus infection.

Infection of goats with goatpox virus triggers host antiviral defense through activation of innate immune signaling.

Avian Tembusu virus infection effectively triggers host innate immune response through MDA5 and TLR3-dependent signaling pathways.