Abstract
The hypothesis that host adaptation in virulent Newcastle disease viruses (NDV) has been accompanied by virulence modulation is reviewed here. Historical records, experimental data, and phylogenetic analyses from available GenBank sequences suggest that currently circulating NDVs emerged in the 1920–1940′s from low virulence viruses by mutation at the fusion protein cleavage site. These viruses later gave rise to multiple virulent genotypes by modulating virulence in opposite directions. Phylogenetic and pathotyping studies demonstrate that older virulent NDVs further evolved into chicken-adapted genotypes by increasing virulence (velogenic-viscerotropic pathotypes with intracerebral pathogenicity indexes [ICPIs] of 1.6 to 2), or into cormorant-adapted NDVs by moderating virulence (velogenic–neurotropic pathotypes with ICPIs of 1.4 to 1.6), or into pigeon-adapted viruses by further attenuating virulence (mesogenic pathotypes with ICPIs of 0.9 to 1.4). Pathogenesis and transmission experiments on adult chickens demonstrate that chicken-adapted velogenic-viscerotropic viruses are more capable of causing disease than older velogenic-neurotropic viruses. Currently circulating velogenic–viscerotropic viruses are also more capable of replicating and of being transmitted in naïve chickens than viruses from cormorants and pigeons. These evolutionary virulence changes are consistent with theories that predict that virulence may evolve in many directions in order to achieve maximum fitness, as determined by genetic and ecologic constraints.
Highlights
Newcastle disease viruses (NDVs), known as avian paramyxoviruses type 1, are members of the genus Orthoavulavirus, species Avian orthoavulavirus 1 in the familyParamyxoviridae
The NDV genome is composed of a single-stranded RNA molecule; it encodes for at least six proteins arranged in a 30 to 50 order: nucleocapsid protein (NP), phosphoprotein (P), matrix protein (M), fusion protein (F), hemagglutinin-neuraminidase (HN), and RNA polymerase [2,3]
Additional evidence for changes in virulence during adaptation to different hosts was demonstrated by Ferreira and others who compared virulence and transmission of NDV of different origins [55]
Summary
Newcastle disease viruses (NDVs), known as avian paramyxoviruses type 1, are members of the genus Orthoavulavirus, species Avian orthoavulavirus 1 in the family. The amino acids at the fusion protein cleavage site interact with secreted host mucosal proteases, which cleave the fusion protein precursor into an active form, making it possible for the virions to attach, infect and replicate in multiple tissues and organs. This enhanced capacity of the cleaved fusion protein is responsible for increased virulence [11,16,17]. Other class II viruses with mesogenic and velogenic neurotropic phenotypes of genotypes VI and XXI are preferentially isolated from wild and domestic Columbiformes [35,36,37,38,39,40] and occasionally from spillover into poultry or other domestic birds. Except for old viruses of genotype V in Viruses 2021, 13, 110 psittacine, there have not been repeated isolations of vvNDV from wild birds; the existence of natural wild bird reservoirs for vvNDV remains to be demonstrated
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