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    • Crystal structure of CD LEL have

    2022-09-21

    Crystal structure of CD81-LEL have revealed the head sub-domain to be implicated in binding to HCV (Kitadokoro et al., 2001). In a study using African green monkey CD81, T163A, F186 L, E188K and D196E mutations disrupted HCV E2 binding (Higginbottom et al., 2000). In our docking studies, T163 and D196 were present in the interaction sites of all four genotypes whereas F186 was found in 1a, 3b and E188 in 1a, 1b and 3b binding sites. Interestingly, while our predictions are supported by studies using 1a, we report results of other genotypes which have not been revealed earlier. Binding energy calculation revealed that E2 from genotype 3a had the highest binding energy compared to all other genotypes followed by 3b, 1b and 1a. Stronger binding energy is believed to result in tighter binding. This may be a reason of higher virulence observed in genotype 3 compared to genotype 1 (Chayama and Hayes, 2011; Shaw et al., 2003) although published literature differ regarding the strength of interaction between CD81 and E2 among genotypes. E2 constructs of HCV 3a generated from patient serum in Glasgow failed to bind CD81 (Shaw et al., 2003). However E2 isolated from other patient serum of genotype 3a exhibited similar binding to CD81 compared to genotypes 1a and 1b (Lavillette et al., 2005). There is however no data available on genotype 3b to the best of our knowledge. Hence our results need to be validated experimentally to conclusively prove the strength of interaction between E2 and CD81.
    Introduction Infectious laryngotracheitis virus (ILTV; Gallid alphaherpesvirus 1) is an alphaherpesvirus that infects chickens, causing an acute upper respiratory tract disease and significant losses to the poultry industry globally (Davison et al., 2009). The disease mainly occurs in densely populated poultry production areas and results in severe production losses due to increased mortality, decreased body weight, loss of egg production and increased susceptibility to other respiratory pathogens (Garcia et al., 2013). A variety of immune responses are generated following infection but not all provide protection against the disease. Early studies on ILTV have suggested that virus neutralizing Cimetidine sale can be detected 5–7 days post-infection (DPI), peak around 21 days and decrease over the next several months (Jordan, 1981.). Local antibodies can be detected in the trachea seven days PI and plateau at 10–28 days PI (Bagust et al., 1986; York et al., 1989a). Antibody titers in serum and mucosal surfaces were linked with the stage of infection (York et al., 1989b). Although antibody and cell-mediated responses are generated against herpesvirus infections, the correlation of humoral immune response in the protection against ILTV infection is debatable (Fahey et al., 1983; Fulton et al., 2000; Leong et al., 1994). There are controversial reports on the role of humoral immune response in protection against herpes simplex viruses (HSV-1 and HSV-2), while antibodies against HSV can mediate prophylactic protection in mice (Sherwood et al., 1996; Zeitlin et al., 1996). Twelve HSV glycoprotein homologs have been identified in the ILTV genome, designated as gK, gN, gH, gB, gC, gJ, gM, gL, gG, gD, gI, and gE, and are considered to be responsible for stimulating humoral and cell-mediated responses (Thureen and Keeler, 2006). Glycoprotein B (UL27) is essential for viral attachment and penetration of host cells. It is involved in cell-to-cell spread and syncytium formation (Lee et al., 2011; Liang et al., 1991). Glycoprotein C (UL44) is a structural protein but non-essential for viral replication in cell culture (Kingsley et al., 1994). It plays a role in viral attachment and virulence. In most alphaherpesviruses, gC mediates viral attachment by interacting with the cellular heparin sulfate receptor (Kingsley et al., 1994). Glycoprotein D (US6) is essential for attachment for most herpesviruses and functions as a receptor binding to susceptible cells (Di Giovine et al., 2011). The gE/gI (US8/US7) heterodimer promotes cell-to-cell spreading of the virus by binding cellular receptors at cell junctions and plays a significant role in cell-to-cell spread of ILTV (Devlin et al., 2006). Glycoprotein G is non-essential but conserved in most alphaherpesviruses. It is not assembled into viral particles but is secreted by infected cells (Helferich et al., 2007). The US5 gene of ILTV encodes glycoprotein J (gJ), which was initially named as gp60 because it was identified as 60 kDa glycoprotein. The only reported function of alphaherpesvirus gJ is its ability to inhibit apoptosis and viral egress, and the mechanisms of these functions are not fully known (Fuchs et al., 2005; Mundt et al., 2011; You et al., 2018)