Introduction:Newcastle Disease (ND), caused by Avian avulavirus 1 (AAvV 1, avulaviruses), is a notifiable disease throughout the world due to the economic impact on trading restrictions and its embargoes placed in endemic regions. The feral birds including aquatic/migratory birds and other wild birds may act as natural reservoir hosts of ND Viruses (NDVs) and may play a remarkable role in the spread of the virus in environment. In addition, other 19 avulaviruses namely: AAvV 2 to 20, have been potentially recognized from feral avian species.Expalantion: Many previous studies have investigated the field prevailing NDVs to adapt a wide range of susceptible host. Still the available data is not enough to declare the potential role of feral birds in transmission of the virus to poultry and/or other avian birds. In view of the latest evidence related to incidences of AAvVs in susceptible avian species, it is increasingly important to understand the potential of viruses to transmit within the domestic poultry and other avian hosts. Genomic and phylogenomic analysis of several investigations has shown the same (RK/RQRR↓F) motif cleavage site among NDV isolates with same genotypes from domestic poultry and other wild hosts. So, the insight of this, various semi-captive/free-ranging wild avian species could play a vital role in the dissemination of the virus, which is an important consideration to control the disease outbreaks. Insufficient data on AAvV 1 transmission from wild birds to poultry and vice versa is the main constraint to understand about its molecular biology and genomic potential to cause infection in all susceptible hosts.Conclusion: The current review details the pertinent features of several historical and contemporary aspects of NDVs and the vital role of feral birds in its molecular epidemiology and ecology.
Since its first report in 1942, peste-des-petits-ruminants virus (PPRV) has caused several epidemics in a wide range of susceptible hosts around the world. In the last 30 years, the evidence of natural and experimental infections and virus isolation were reported from novel but unusual hosts such as camel, cattle, buffalo, dogs, Asiatic lion and pigs. In addition, PPRV in a potential vector, biting midges (Culicoides imicola), has been reported. Either presented as clinical and/or subclinical infections, the presence of the virus in an extended range of susceptible hosts highlights the cross-species transmission and supports the hypothesis of an endemic circulation of PPRV among susceptible hosts. However, the potential role of large ruminants, camels and unusual hosts for PPRV epidemiology is still obscure. Therefore, there is a need for molecular and epidemiological investigations of the disease among usual and unusual hosts to achieve the goals of disease control and eradication programmes initiated by national and international organisations, such as the FAO and OIE. This review is the first to summarise the scattered data on PPR in large ruminants, camels and unusual hosts to obtain the global scientific communities' attention for further research on epidemiological aspects, not only in its native hosts, but also in large ruminants, camels and other unusual hosts.
A string of complete genome sequences of Small ruminant morbillivirus (SRMV) have been reported from different parts of the globe including Asia, Africa and the Middle East. Despite individual genome sequence-based analysis, there is a paucity of comparative genomic and evolutionary analysis to provide overarching and comprehensive evolutionary insights. Therefore, we first enriched the existing database of complete genome sequences of SRMVs with Pakistan-originated strains and then explored overall nucleotide diversity, genomic and residue characteristics, and deduced an evolutionary relationship among strains representing a diverse geographical region worldwide. The average number of pairwise nucleotide differences among the whole genomes was found to be 788.690 with a diversity in nucleotide sequences (0.04889 ± S.D. 0.00468) and haplotype variance (0.00001). The RNAdependent-RnA polymerase (L) gene revealed phylogenetic relationship among SRMVs in a pattern similar to those of complete genome and the nucleoprotein (N) gene. Therefore, we propose another useful molecular marker that may be employed for future epidemiological investigations. Based on evolutionary analysis, the mean evolution rate for the complete genome, N, P, M, F, H and L genes of SRMV was estimated to be 9.953 × 10-4 , 1.1 × 10-3 , 1.23 × 10-3 , 2.56 × 10-3 , 2.01 × 10-3 , 1.47 × 10-3 and 9.75 × 10-4 substitutions per site per year, respectively. A recombinant event was observed in a Pakistan-originated strain (KY967608) revealing Indian strains as major (98.1%, KR140086) and minor parents (99.8%, KT860064). Taken together, outcomes of the study augment our knowledge and current understanding towards ongoing phylogenomic and evolutionary dynamics for better comprehensions of SRMVs and effective disease control interventions.
Peste des petits ruminants virus (PPRV) infects a wide range of domestic and wild ruminants, and occasionally unusual hosts such as camel, cattle and pig. Given their broad host-spectrum and disease endemicity in several developing countries, it is imperative to elucidate the viral evolutionary insights for their dynamic pathobiology and differential host-selection. For this purpose, a dataset of all available (n=37) PPRV sequences originating from wild and unusual hosts was composed and in silico analysed. Compared to domestic small ruminant strains of same geographical region, phylogenomic and residue analysis of PPRV sequences originating from wild and unusual hosts revealed a close relationship between strains. A lack of obvious difference among the studied sequences and deduced residues suggests that these are the host factors that may play a role in their susceptibility to PPRV infection, immune response, pathogenesis, excretion patterns and potential clinical signs or resistance to clinical disease. Summarizing together, the comparative analysis enhances our understanding towards molecular epidemiology of the PPRV in wild and unusual hosts for appropriate intervention strategies particularly at livestock-wildlife interface.
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