This study reported the development and characterisation of bio-nanocomposite films based on the polyvinyl alcohol (PVA) reinforced with cellulose nanofibres (CNFs) of different concentrations (1-5 wt%), isolated from pineapple leaf fibre via high-shear homogenisation and ultrasonication. The PVA film and bio-nanocomposite were prepared using a solution casting method. The PVA film and bio-nanocomposite samples were characterized using FE-SEM, XRD, FTIR spectroscopy, UV-vis spectroscopy in transmission mode, TGA, and DTG. Mechanical properties (tensile strength and strain at break) were also determined and statistical analysis was applied as well. With the incorporation of CNFs, the mechanical properties of the bio-nanocomposite were found to be significant (p ≤ 0.05), particularly the 4 wt% CNF bio-nanocomposite showed optimum properties. The tensile strength, CI, and thermal stability of this film were 28.9 MPa (increased by 28.2%), 78.7% (increased by 5.2%), and 341.8 °C (increased by 1.6%), respectively, compared to the pure PVA film. These characteristics imply that the bio-nanocomposite film has prospects as a promising material for biopackaging.
Type I interferon (IFN-α/β) is a fundamental antiviral defense mechanism. Mouse models have been pivotal to understanding the role of IFN-α/β in immunity, although validation of these findings in humans has been limited. We investigated a previously healthy child with fatal encephalitis after inoculation of the live attenuated measles, mumps, and rubella (MMR) vaccine. By targeted resequencing, we identified a homozygous mutation in the high-affinity IFN-α/β receptor (IFNAR2) in the proband, as well as a newborn sibling, that rendered cells unresponsive to IFN-α/β. Reconstitution of the proband's cells with wild-type IFNAR2 restored IFN-α/β responsiveness and control of IFN-attenuated viruses. Despite the severe outcome of systemic live vaccine challenge, the proband had previously shown no evidence of heightened susceptibility to respiratory viral pathogens. The phenotype of IFNAR2 deficiency, together with similar findings in STAT2-deficient patients, supports an essential but narrow role for IFN-α/β in human antiviral immunity.