Psittacine beak and feather disease (PBFD) is recognized as a threat for endangered psittacine birds in Australia, New Zealand and South Africa. Several diagnostic methods for the detection of beak and feather disease virus (BFDV) infection have been developed but there are few studies comparing the relative merits or sensitivity and specificity of each diagnostic test. In this report, the results of PCR, haemagglutination (HA) and haemagglutination inhibition (HI) testing of diagnostic samples collected from 679 samples from a range of psittacine bird species suspected of being infected with BFDV are summarized and compared. There was a strong agreement (kappa = 0?757; P<0?0001) between PCR and HA testing of feather samples and PCR-negative birds were 12?7 times more likely to have HI antibody than PCR-positive birds. False-positive HA results with titres up to 1 : 320 were identified in six feather samples that were PCR negative; the haemagglutination detected in these samples was not inhibited by anti-BFDV antisera and was removed by filtration through a 0?22 mm filter. Similarly, one false-negative PCR result was detected in a feather sample that had a high HA titre (>1 : 40 960) and four false-positive PCR results were detected in a batch of four feather samples. Of 143 birds that were feather PCR positive, only two had detectable HI antibody, and these birds were also feather HA negative, suggesting that they were developing immunity to recent infection. All birds with HI antibody were negative on feather HA testing. The assays confirmed BFDV infection in two endangered swift parrots (Lathamus discolor) and phylogenetic analysis of the sequence data generated from ORF V1 of these isolates provide further evidence of BFDV genotypes clustering in parallel with the Loriidae, Cacatuidae and Psittacidae.

Large contact surfaces of protein–protein interactions (PPIs) remain to be an ongoing issue in the discovery and design of small molecule modulators. Peptides are intrinsically capable of exploring larger surfaces, stable, and bioavailable, and therefore bear a high therapeutic value in the treatment of various diseases, including cancer, infectious diseases, and neurodegenerative diseases. Given these promising properties, a long way has been covered in the field of targeting PPIs via peptide design strategies. In silico tools have recently become an inevitable approach for the design and optimization of these interfering peptides. Various algorithms have been developed to scrutinize the PPI interfaces. Moreover, different databases and software tools have been created to predict the peptide structures and their interactions with target protein complexes. High-throughput screening of large peptide libraries against PPIs; “hotspot” identification; structure-based and off-structure approaches of peptide design; 3D peptide modeling; peptide optimization strategies like cyclization; and peptide binding energy evaluation are among the capabilities of in silico tools. In the present study, the most recent advances in the field of in silico approaches for the design of interfering peptides against PPIs will be reviewed. The future perspective of the field and its advantages and limitations will also be pinpointed.

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Glioblastoma belongs to the most aggressive type of cancer with a low survival rate that is characterized by the ability in forming a highly immunosuppressive tumor microenvironment. Intercellular communication are created via exosomes in the tumor microenvironment through the transport of various biomolecules. They are primarily involved in tumor growth, differentiation, metastasis, and chemotherapy or radiation resistance. Recently several studies have highlighted the critical role of tumor-derived exosomes against immune cells. According to the structural and functional properties, exosomes could be essential instruments to gain a better molecular mechanism for tumor understanding. Additionally, they are qualified as diagnostic/prognostic markers and therapeutic tools for specific targeting of invasive tumor cells such as glioblastomas. Due to the strong dependency of exosome features on the original cells and their developmental status, it is essential to review their critical modulating molecules, clinical relevance to glioma, and associated signaling pathways. This review is a non-clinical study, as the possible role of exosomes and exosomal microRNAs in glioma cancer are reported. In addition, their content to overcome cancer resistance and their potential as diagnostic biomarkers are analyzed.

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Spike glycoprotein (Sgp) is liable for binding of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to the host receptors. Since Sgp is the main target for vaccine and drug designing, elucidating its mutation pattern could help in this regard. This study is aimed at investigating the correspondence of specific residues to the SgpSARS-CoV-2 functionality by explorative interpretation of sequence alignments. Centrality analysis of the Sgp dissects the importance of these residues in the interaction network of the RBD-ACE2 (receptor-binding domain) complex and furin cleavage site. Correspondence of RBD to threonine500 and asparagine501 and furin cleavage site to glutamine675, glutamine677, threonine678, and alanine684 was observed; all residues are exactly located at the interaction interfaces. The harmonious location of residues dictates the RBD binding property and the flexibility, hydrophobicity, and accessibility of the furin cleavage site. These species-specific residues can be assumed as real targets of evolution, while other substitutions tend to support them. Moreover, all these residues are parts of experimentally identified epitopes. Therefore, their substitution may affect vaccine efficacy. Higher rate of RBD maintenance than furin cleavage site was predicted. The accumulation of substitutions reinforces the probability of the multi-host circulation of the virus and emphasizes the enduring evolutionary events.