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We report 1.3% (19/1,511) of Egyptian rousette bats (ERBs) in Uganda and Sierra Leone were co-infected with different combinations of Marburg, Sosuga, Kasokero, or Yogue viruses. To prevent infection by those viruses, we recommend avoiding ERB-populated areas, avoiding ERBs and ERB-contaminated objects, and thoroughly washing harvested fruits before consumption.

The protein C is a small viral protein encoded in an overlapping frame of the P gene in the subfamily Orthoparamyxovirinae. This protein, expressed by alternative translation initiation, is a virulence factor that regulates viral transcription, replication, and production of defective interfering RNA, interferes with the host-cell innate immunity systems and supports the assembly of viral particles and budding. We expressed and purified full-length and an N-terminally truncated C protein from Tupaia paramyxovirus (TupV) C protein (genus Narmovirus). We solved the crystal structure of the C-terminal part of TupV C protein at a resolution of 2.4 Å and found that it is structurally similar to Sendai virus C protein, suggesting that despite undetectable sequence conservation, these proteins are homologous. We characterized both truncated and full-length proteins by SEC-MALLS and SEC-SAXS and described their solution structures by ensemble models. We established a mini-replicon assay for the related Nipah virus (NiV) and showed that TupV C inhibited the expression of NiV minigenome in a concentration-dependent manner as efficiently as the NiV C protein. A previous study found that the Orthoparamyxovirinae C proteins form two clusters without detectable sequence similarity, raising the question of whether they were homologous or instead had originated independently. Since TupV C and SeV C are representatives of these two clusters, our discovery that they have a similar structure indicates that all Orthoparamyxovirine C proteins are homologous. Our results also imply that, strikingly, a STAT1-binding site is encoded by exactly the same RNA region of the P/C gene across Paramyxovirinae, but in different reading frames (P or C), depending on which cluster they belong to.

Newcastle disease (ND) is a highly contagious viral disease of poultry causing significant economic losses worldwide. Vaccination is considered the most reliable approach to curb the economic menace that is ND, but the thermolabile nature of Newcastle disease virus (NDV) vaccination poses a significant threat to its protective efficacy. This study aimed to profile the thermostability of NDV isolates from duck (As/Km/19/44) and parrot (As/WB/19/91) and evaluate their immunogenic potential in chicks. Fusion protein cleavage site (FPCS) and phylogenetic analysis demonstrated the lentogenic nature of both the isolates/strains and classified them as class II genotype II NDV. The characterized NDV isolates were adapted in specific-pathogen-free (SPF) chicks by serially passaging. Biological pathogenicity assessment of chicken-adapted As/Km/19/44 (PSD44C) and As/WB/19/91 (PSP91C) revealed both the isolates to be avirulent with a mean death time (MDT) of more than 90 h and an intracerebral pathogenicity index (ICPI) ranging from 0.2 to 0.4. Both of the NDV isolates displayed varied thermostability profiles. PSD44C was the most thermostable strain as compared to PSP91C and the commercially available LaSota vaccine strain. The immunogenicity of PSD44C and LaSota was significantly higher than PSP91C. Based on these results, it is concluded that NDV isolate PSD44C is more thermostable and immunogenic when administered intraocularly without any adverse effects. Therefore, PSD44C is suitable for further research and vaccine development.

Peste des Petits Ruminants (PPR) is a highly contagious viral disease of small ruminants that severely threatens rural livelihoods and global food security. Under the Global Framework for the Progressive Control of Transboundary Animal Diseases (GF-TADs), the international animal health community has set the ambitious goal of eradicating PPR by 2030. However, significant disparities persist in the progression of PPR control across regions. This scoping review assesses the setbacks, deviations, and progress of 42 countries in Eastern, Western, and Northern Africa, as well as West Eurasia, toward achieving official freedom-from-PPR status. Progress was evaluated across key areas using the stepwise PPR Global Control and Eradication Strategy (GCES) approach and the PPR Monitoring and Assessment Tool (PMAT). The eligibility criteria included PubMed peer-reviewed studies, FAO/WOAH reports, presentations, guidelines, and country/region-specific PPR control plans from 2014 through 2024. The data are generated using qualitative and quantitative analyses, including spatial mapping and GCES stepwise progress evaluation. The findings reveal that many (31%) countries in the assessed regions remain in Stage 1 of the Progressive Stepwise Approach, whereas 59.5% have reached Stages 2 and 3, and only 4.8% are in Stage 4. Countries in Western Eurasia have achieved significant progress towards PPR control, with countries achieving PPR-free status, whereas, compared to Eastern and Northern Africa, the Western African region remains in the early control stages due to infrastructure gaps and resource constraints. Additionally, the recent suspension of PPR-free status in Romania, Greece and Hungary following disease emergence underscored vulnerabilities in historically free countries. The analysis results reiterate the critical role of regional collaboration, surveillance tools, and the integration of wildlife monitoring in advancing PPR control. These insights provide actionable pathways to addressing persistent barriers, highlighting the importance of adaptable, evidence-based approaches in achieving the global goal of PPR eradication by 2030.

The family includes a number of negative RNA viruses known for their wide host range and significant zoonotic potential. In recent years, there has been a surge in the identification of emerging zoonotic paramyxoviruses, particularly those hosted by bat species, which serve as key reservoirs. Among these, the genera Henipavirus and Pararubulavirus are of particular concern. Henipaviruses, including the highly pathogenic Hendra and Nipah viruses, have caused severe outbreaks with high mortality rates in both humans and animals. In contrast, zoonotic pararubulaviruses such as the Menangle virus typically induce mild symptoms or remain asymptomatic in human hosts. This review summarizes current knowledge on the evolution, ecology, and epidemiology of emerging zoonotic paramyxoviruses, focusing on recently discovered viruses and their potential to cause future epidemics. We explore the molecular mechanisms underlying host-switching events, viral replication strategies, and immune evasion tactics that facilitate interspecies transmission. In addition, we discuss ecological factors influencing virus emergence, including changes in bat populations and habitats and the role of wildlife-human interfaces. We also examine the public health impact of these emerging viruses, underlining the importance of enhanced surveillance, developing improved diagnostic tools, and implementing proactive strategies to prevent potential outbreaks. By providing a comprehensive overview of recent advances and gaps in knowledge, this review aims to inform future research directions and public health policies related to zoonotic paramyxoviruses.

The paramyxovirus receptor-binding protein (RBP) plays a primary role in determining cell and species tropism. Here, we study the RBPs of jeilongviruses, a group of paramyxoviruses that present a distinctive RBP that encodes an elongated C-terminal region. While the jeilongviral RBP structurally categorizes with paramyxoviral RBPs that interact with sialic acid during host-cell entry, the unusually long C-terminal domain was found to sterically occlude the associated binding site, suggesting that the molecule has developed strategies for autoinhibition of receptor interactions. These data expand our understanding of the architectural space occupied by paramyxoviral RBPs and the structural elaborations that may be incorporated into the paramyxovirus genome to modulate native functionality.

Background Canine distemper virus (CDV), currently termed Canine morbillivirus , is an extremely contagious disease that affects dogs. It is identified as a multiple cell tropism pathogen, and its host range includes a vast array of species. As a member of Mononegavirales , CDV has a negative, single-stranded RNA genome, which encodes eight proteins. Main body Regarding the molecular pathogenesis, the hemagglutinin protein (H) plays a crucial role both in the antigenic recognition and the viral interaction with SLAM and nectin-4, the host cells’ receptors. These cellular receptors have been studied widely as CDV receptors in vitro in different cellular models. The SLAM receptor is located in lymphoid cells; therefore, the infection of these cells by CDV leads to immunosuppression, the severity of which can lead to variability in the clinical disease with the potential of secondary bacterial infection, up to and including the development of neurological signs in its later stage. Conclusion Improving the understanding of the CDV molecules implicated in the determination of infection, especially the H protein, can help to enhance the biochemical comprehension of the difference between a wide range of CDV variants, their tropism, and different steps in viral infection. The regions of interaction between the viral proteins and the identified host cell receptors have been elucidated to facilitate this understanding. Hence, this review describes the significant molecular and cellular characteristics of CDV that contribute to viral pathogenesis.

Emerging RNA virus infections are a growing concern among domestic poultry industries due to the severe impact they can have on flock health and economic livelihoods. Avian paramyxoviruses (APMV; avulaviruses, AaV) are pathogenic, negative-sense RNA viruses that cause serious infections in the respiratory and central nervous systems. APMV was detected in multiple avian species during the 2017 wild bird migration season in Ukraine and studied using PCR, virus isolation, and sequencing. Of 4090 wild bird samples collected, mostly from southern Ukraine, eleven isolates were grown in ovo and identified for APMV serotype by hemagglutinin inhibition test as: APMV-1, APMV-4, APMV-6, and APMV-7. To build One Health’s capacity to characterize APMV virulence and analyze the potential risks of spillover to immunologically naïve populations, we sequenced virus genomes in veterinary research labs in Ukraine using a nanopore (MinION) platform. RNA was extracted and amplified using a multiplex tiling primer approach to specifically capture full-length APMV-1 (n = 5) and APMV-6 (n = 2) genomes at high read depth. All APMV-1 and APMV-6 fusion (F) proteins possessed a monobasic cleavage site, suggesting these APMVs were likely low virulence, annually circulating strains. Utilization of this low-cost method will identify gaps in viral evolution and circulation in this understudied but important critical region for Eurasia.

Paramyxoviruses represent a family of RNA viruses causing significant human diseases. These include measles virus, the most infectious virus ever reported, in addition to parainfluenza virus, and other emerging viruses. Paramyxoviruses likely share common replication machinery but their mechanisms of RNA biosynthesis activities and details of their complex polymerase structures are unknown. Mechanistic and functional details of a paramyxovirus polymerase would have sweeping implications for understanding RNA virus replication and for the development of new antiviral medicines. To study paramyxovirus polymerase structure and function, we expressed an active recombinant Nipah virus (NiV) polymerase complex assembled from the multifunctional NiV L protein bound to its phosphoprotein cofactor. NiV is an emerging highly pathogenic virus that causes severe encephalitis and has been declared a global public health concern due to its high mortality rate. Using negative-stain electron microscopy, we demonstrated NiV polymerase forms ring-like particles resembling related RNA polymerases. We identified conserved sequence elements driving recognition of the 3'-terminal genomic promoter by NiV polymerase, and leading to initiation of RNA synthesis, primer extension, and transition to elongation mode. Polyadenylation resulting from NiV polymerase stuttering provides a mechanistic basis for transcription termination. It also suggests a divergent adaptation in promoter recognition between pneumo- and paramyxoviruses. The lack of available antiviral therapy for NiV prompted us to identify the triphosphate forms of R1479 and GS-5734, two clinically relevant nucleotide analogs, as substrates and inhibitors of NiV polymerase activity by delayed chain termination. Overall, these findings provide low-resolution structural details and the mechanism of an RNA polymerase from a previously uncharacterized virus family. This work illustrates important functional differences yet remarkable similarities between the polymerases of nonsegmented negative-strand RNA viruses.

Human metapneumovirus (hMPV) is an important cause of respiratory disease in immunocompromised individuals, yet hMPV infection has not been modeled before in immunocompromised animals. In this work, cotton rats S. hispidus immunosuppressed by cyclophosphamide were infected with hMPV, and viral replication and pulmonary inflammation in these animals were compared to those in normal hMPV-infected S. hispidus. The efficacy of prophylactic and therapeutic administration of the anti-hMPV antibody MPV467 was also evaluated. Immunosuppressed animals had higher pulmonary and nasal titers of hMPV on day 5 post-infection compared to normal animals, and large amounts of hMPV were still present in the respiratory tract of immunosuppressed animals on days 7 and 9 post-infection, indicating prolonged viral replication. Immunosuppression was accompanied by reduced pulmonary histopathology in hMPV-infected cotton rats compared to normal animals; however, a delayed increase in pathology and pulmonary chemokine expression was seen in immunosuppressed cotton rats. Prophylactic and therapeutic MPV467 treatments protected both upper and lower respiratory tracts against hMPV infection. The lung pathology and pulmonary expression of IP-10 and MIP-1α mRNA were reduced by therapeutic MPV467 administration. These results indicate that immunosuppressed cotton rats represent a useful model for studying hMPV pathogenesis and for evaluating therapeutics that could alleviate hMPV-induced disease in immunocompromised subjects.