This study demonstrates the capacity of HM-γ-PGA treatment to significantly protect murine macrophage cells (RAW 264.7 cells) against NDV infection. Such protection can be explained by the induction of antiviral state of HM-γ-PGA in RAW 264.7 cells via TLR4-mediated IRF-3, IRF-7, IFN-β, and IFN-related gene induction as shown in time-dependent changes in mRNA expression confirmed by polymerase chain reaction (PCR). Moreover, the present research also showed that HM-γ-PGA can induce proinflammatory cytokine secretion in RAW 264.7 as measured by enzyme-linked immunosorbent assay (ELISA). Therefore, our findings suggest that HM-γ-PGA can be a potential antiviral substance that can inhibit NDV infection through its stimulation of antiviral state on RAW 264.7 cells. These results have been consistent with the previous studies showing that HM-γ-PGA can protect RAW 264.7 cells and mice against influenza infection. However, it should be noted that although murine macrophage cells are susceptible to NDV, they are not the natural host cells of the virus; thus further in vivo and in vitro studies involving chicken and chicken immune cells are needed to fully assess the efficacy and applicability of HM-γ-PGA in the poultry industry. 1. Introduction Newcastle disease virus (NDV) is a member of the Paramyxoviridae family under the genus Avulavirus [1, 2] and is currently designated as avian paramyxovirus virus serotype 1 (APMV-1) . According to the Office International des Epizooties (OIE) in 2009, NDV strains can be classified into five pathotypes according to the clinical signs shown by the affected chickens, namely, viscerotropic velogenic (high mortality and hemorrhagic intestinal lesions), neurotropic velogenic (high mortality, respiratory, and nervous signs), mesogenic (low mortality, respiratory signs with occasional nervous signs), lentogenic (subclinical or mild infection), and asymptomatic enteric (subclinical enteric infection) ones . Newcastle disease remains prevalent worldwide, though a number of live and inactivated NDV vaccines are available to control the disease [5, 6]. However, the currently available commercial vaccines have their limitations and one of them is the absence of genetic markers for serological differentiation between vaccinated and naturally infected birds. There are also reports suggesting that the types of NDV strains that have been identified circulating in poultry already showed major antigenic drift. Thus, there is a need for better NDV vaccines which can solve such problems, wherein viral vector vaccines prove to be a
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