Abstract
Canine distemper (CD), caused by the CDV variant strain with HI542N/Y549H, has become an epidemic in fur-bearing animals in China since 2012. To well understand the genomic and replicated characteristics of the CDV variants, we determined the viral growth kinetics and completed the genome sequences of two CDV strains, namely SDZC(17)M2 and LNDL(17)M4, isolated from CDV-infected minks from Shandong and Liaoning province in China, in 2017. SDZC(17)M2 showed higher viral titers and extensive syncytia in BHK-minkSLAM (BMS) cells than LNDL(17)M4. Although both two strains belong to the Asia-1 genotype and clustered an independent clade in the phylogenetic tree, SDZC(17)M2, harboring I542N/Y549H substitutions in the H protein, shared high identity (99.3–99.6% nt) with the other variant strains, whereas LNDL(17)M4, with the only Y549H substitution, shared a lower identity (97.7%–97.9% nt) with the other variant strains. Furthermore, a novel R223K substitution was identified in the conserved cleavage site (RRQRR → RRQKR) of the F protein in the SDZC(17)M2 strain. However, it which did not significantly affect the cell to cell fusion activity when combined with the CDV H/minkSLAM in BHK-21 cells. The key variations in the genome contributed to the virulence and the evolutionary trend need to be determined in the future.
Highlights
Canine distemper (CD) is a highly contagious, often fatal, multisystemic disease caused by canine distemper virus (CDV) in a wide range of mammalian hosts, with clinical symptoms including conjunctivitis, anorexia, diarrhea, lymphopenia, and encephalitis [1]
BMS cells were infected with viruses at a multiplicity of infection of 0.1, and cell-associated progeny viruses were collected at the designated time points
The results showed that the CDV F R223K substitution resulted in cell fusion when combined with LNDL[17]M4H or SDZC[17]M2H (Figure 4A)
Summary
Canine distemper (CD) is a highly contagious, often fatal, multisystemic disease caused by canine distemper virus (CDV) in a wide range of mammalian hosts, with clinical symptoms including conjunctivitis, anorexia, diarrhea, lymphopenia, and encephalitis [1]. The P gene encodes two non-structural proteins, C and V, which modulate the virulence and immune suppression activities of CDV by inhibiting the induction of the host’s type I and II interferon [5]. The matrix protein (M) has a significant impact on the budding of virus particles [6], while the major antigenic proteins, the haemagglutinin (H) and the fusion (F), can induce immune responses that protect the host from viral infection [7, 8]. The UTRs between the M and F gene play an important role in modulating F protein expression and CDV virulence [11]. CDV enters the susceptible hosts, by recognizing and binding to the host’s receptors, initiating the early stages of infection. Two molecules, namely signaling lymphocytic activation molecule (SLAM/CD150) and poliovirus receptorrelated 4(Nectin4/PVRL4) have been identified as the cellular receptors of CDV [12, 13]
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