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Blue Tongue Virus (BTV) in cattle and sheep - Coggle Diagram

- - - - Host become infected from the saliva from a biting midge
        
        Horizontal & Vertical transmission route between ruminant species have been documented
        
        BTV-1, BTV-2, BTV-8 under experimental conditions spread between naiive ruminants within a herd with the probable transmission route through to be close proximity and or shared feed/water troughs (Rojas et al., 2021)
      - Culicoides species feed on
        viraemic animals
        
        Viral replication takes place within the insects salivary glands over 6-8 days
        Once exposed to BTV strain the insect can transmit disease for the rest of its life - up to three months (Steyn et al., 2016)
        
        Geographical maps indicating the basic reproduction number can be used to identify areas of higher risk after disease introduction. these include areas of vector abundance. (Hartemink et al., 2009)
  - - - Endothelial damage resulting from apoptosis, damages the blood vessels
        
        This leads to haemorrhages and oedema as damages vessels become more leaky
        
        Results of this include poor oxygen delivery & tissue injury
    - - Peracute cases die within 7-9 days with severe pulmonary edema resulting in asphyxiation - (Lear Andrea, 2025)
      - Chronic cases sheep may die 3-5 weeks after infection due to bacterial complications (Lear Andrea, 2025)
        
        Seroprevalence tests carried out in china greatly affected by BTV (Zhong et al., 2024) revealed relatively low in sheep 36.8% compared to cattle 57.1% within the Yunnan province (Zhong et al., 2024b). BTV effect more sheep than cattle within China (Santman-Berends et al., 2026) this results suggest many sheep die before beginning antibody production, Matching the acute nature of BTV within sheep.
      - Within cattle disease is usually sub clinical, however disease similar to sheep can occur (Dubovi et al., 2011)
      - Clinical study of six native sheep intradermally infected with BTV serotype 24 and then euthanised at 4,7,11,16,45 and 60 days post inoculation (Vineetha et al., 2026)
        
        All animals infected presented with pyrexia, conjunctival and oral mucosal congestion, cyanosis of tongue, serous to catarrhal nasal discharge, and viremia. Gross pathological lesions were observed in the lymph nodes, lungs, and kidneys, with the lymph nodes being enlarged, edematous, and hemorrhagic (Vineetha et al., 2026)
        
        At seven days post inoculation Subintimal hemorrhage at the base of the pulmonary artery (pathognomonic lesion of BT) was observed (Vineetha et al., 2026)
        
        Humoral immune response was significantly high at 5, 11, 16, 21, 45, and 60 DPI (Vineetha et al., 2026)
        
        Cell-mediated immune response-like kinetics of CD4+ and CD8+ T lymphocytes showed a sharp decline during the early stage and an increase of CD8+ T lymphocytes during later stages of infection. (Vineetha et al., 2026)
        
        Study showed the moderate progression of the disease and enhanced virulence of the BTV-24 serotype (Vineetha et al., 2026)
    - - In rare cases and in severe cases, the
        tongue may become cyanotic through vascular
        compromise, hence the name “bluetongue
    - - BTV 8 presents with the unique ability of trans placental infection possibly adapted from live attenuated vaccines (van der Sluijs et al., 2011)
      - Live attenuated vaccines are available to most serotypes in America and south Africa, these provide strong stereotypic immunity however has been associated with foetal death and abnormalities, especially those propagated in egg cells (Dubovi et al., 2011)
  - - - Infection by the BTV particle is established when the inner capsid of the double-capsid particle, the “core”, translocates across the endosomal membrane following virus uptake. (Roy Polly)
      - VP2 can act as an environmental senor mediating cell attatchement between cell and virus, mediated by the Claritin coated pit pathways. VP5 also play a role within cell fusion (Patel and Roy, 2013)
      - Host humoral response strongly targets the VP2 protein exerting selection pressure on virus to mutate to evade immune system (Patel and Roy, 2013). This is the major driving factor in the evolution of many different BTV serotypes and strains (Bissett and Roy, 2024)
        
        pressure on VP2 promotes emergence of novel serotypes, requiring continual vaccine adaptation and rapid molecular surveillance
      - Binding of BTV to mammalian cells appear to be mediated by VP2 with studies suggest binding and penetration of the cell occurs within 10 mins
        
        VP2 Serotype specific
      - Inoculated into the blood following blood meal from biting midge genus Culicoides primary infection occurs in the endothelial cells and mononuclear phagocytes namely dendritic cells present in the lymph node draining. (Patel and Roy, 2013)
      - Replication prinicply in the macrophages, dendritic cells and vascular endothelium (Dubovi et al., 2011)
      - Infects mammalian and insect cells although each may be facilitated through different processes.
      - Removal of the BTV outer caspid is essential for the activation of the virus transcriptase, allowing the core particles that are released into the host cell cytoplasm to synthesis viral mRNAs and initiate replication.(Matsuo and Roy, 2009)
- - - - BTV constantly modifying within body VP2 contstantly adapting and changing, immune system has to relearn target takes time infection continues
  - - - Functioning normally activated T cells within the lymph node through various pathogen receptors capable of recognising viral genetic material. Additionally involved in antigen specific B cell production (Rodríguez-Martín et al., 2021)
      - In the presence of BTV dendritic cells are shown to act as viral transport from biting site to Lymphnode where viral replication occurs (Rodríguez-Martín et al., 2021)
      - In this case BTV targets follicular dendritic cells impairing antibody responses
      - Similarly Conventional dendritic cells have been shown to provide a primary source of dissemination for infection. BTV inoculation promotes recruitment of cDCs to sheep skin and lymph node (secondary dissemination) providing cellular targets for infection - (Hemati et al., 2009)
      - Primary infection of dendritic cells has no adverse effect of functionality or physiology, this initially benefits the virus as no abnormalities are detected by immune system and thus response is delayed (Hemati et al., 2009)
      - Critical link between innate and adaptive immune response - (Steinman and Hemmi, 2006)
    - - CD4+ T-cells are more susceptible to infection than CD8+ T-cells in sheep and cattle (Rodríguez-Martín et al., 2021
      - This type of cellular immunity provides only partial protection, however, cross reactive between serotypes (Rodríguez-Martín et al., 2021)
- - - - Effective control achieved through vaccine use, reliant on correct usage. This recquired owner and veterinary compliance. Incomplete vaccination corses does not establish same levels of immunity (Santman-Berends, van den Brink, K. M. J. A. et al., 2026)
    - - Vaccination is highly effective for controlling specific BTV serotypes at a population level, but its overall success is limited by the emergence of new serotypes, requiring continuous surveillance and updated vaccination strategies.
        
        Governmental support through national surveys, mandatory reporting and lab work help identify high risk serotypes within areas - allowing for adequate vaccination
    - - These are safer than live attenuated vaccines with no risk of reassortment, however still under development and more expensive.
      - Possible issue with this as BTV has partial resistance to cellular response, animal therefore remain partially vulnerable
      - T- cells susceptibility to BTV infection suggest a vaccine that relies on cell mediated immunity without antibody production may have flaws
    - - Classical vaccines such as live attenuated and inactivated are serotype specific (Rojas, José M. et al., 2021)
        
        Live attenuated vaccines provide strong long-lasting immunity whereas inactivated vaccines may require booster or revaccinations this adds to cost. However, as seen within the BTV-8 serotype there is a risk of reassortment associated with live attenuated vaccines, this resulted in vertical cross placental transmission within BTV -8
        
        Although live attenuated vaccines induce stronger immunity, inactivated vaccines are more suitable for large-scale eradication programmes due to reduced reassortment risk
        
        Serotype specificity is also an issue regarding BTV vaccination as identification of correct serotype is required before to ensure appropriate vaccine is used, this can be achieved using PCR.
        
        Targets VP2 - Because neutralising antibodies primarily target VP2, antigenic variation between serotypes limits cross-protection, necessitating serotype-matched vaccination and continuous surveillance
      - in
  - - - Areas of greater vector abundance more at risk
      - Can monitor travel patterns of vectors
    - - Lead to identification of serotype presence
      - Allowing targeted vaccine administration
        
        Particularly important due to cross serotype protection limitations