Canine parvovirus type 2c in Vietnam continues to produce distinct descendants with new mutations restricted to Vietnamese variants

Author(s):  
Huong Thi Thanh Doan ◽  
Xuyen Thi Kim Le ◽  
Roan Thi Do ◽  
Khue Thi Nguyen ◽  
Thanh Hoa Le
Author(s):  
Huong Thi Thanh Doan ◽  
Xuyen Thi Kim Le ◽  
Roan Thi Do ◽  
Khue Thi Nguyen ◽  
Thanh Hoa Le

2021 ◽  
Author(s):  
THANH HOA LE ◽  
Huong Thi Thanh Doan ◽  
Xuyen Thi Kim Le ◽  
Roan Thi Do ◽  
Khue Thi Nguyen

Abstract The complete sequence for viral protein 2 (VP2) of canine parvovirus (CPV) was obtained from 33 isolates collected from dogs with clinical symptoms and a vaccine in Vietnam from Mar 2017– June 2019. Molecular analysis revealed the descent evolution in CPV-2c-“new”, forming a “new var.” sub-lineage of the substantial 5G, 447M mutations restricted to the Vietnamese isolates in the epitope stretches. These were found besides the common 80R, 87L, 93N, 101T, 103A, 232I, 267Y, 297A, 300G, 305Y, 323N, 324I, 334A, 341P, 370R, 426E, 440T, 447I, 555V, 564S, and 568G typical to the “new” CPV-2c. The novel 447M mutation seemed to emerge in recent years in Vietnam and was present in 38 of 58 CPV-2c strains isolated from December 2016 to June 2019 by our retrospective analysis, counting for 65.5%. With strong nodal support (98%), the topology of the phylogenetic tree revealed the substantially distinct Vietnamese sub-lineage of 2c-“new-var.” (5G/426E/447M) separated from the Vietnamese 2c-“new” (5G/426E/447I), within the 2c-(Asia)/Asia-2c. The Asia-2c strains of Vietnam were grouped with the recent Thai, Chinese, Mongolian, Taiwanese, Korean, and the Asian variants newly imported into Italy, Egypt, and Nigeria from Asia. The changes of amino acids in the epitope stretch in VP2 have effective alteration not only on the continual formation of substantial sub- or new genotypic variants but may be of subjects for antigenicity/immunogenicity and virulence to the CPV-2 strains and vaccine failure worldwide.


1995 ◽  
Vol 69 (11) ◽  
pp. 7274-7277 ◽  
Author(s):  
J I Casal ◽  
J P Langeveld ◽  
E Cortés ◽  
W W Schaaper ◽  
E van Dijk ◽  
...  

2020 ◽  
Vol 32 (3) ◽  
pp. 463-466 ◽  
Author(s):  
Arno Wünschmann ◽  
Robert Lopez-Astacio ◽  
Anibal G. Armien ◽  
Colin R. Parrish

A juvenile raccoon ( Procyon lotor) was submitted dead to the Minnesota Veterinary Diagnostic Laboratory for rabies testing without history. The animal had marked hypoplasia of the cerebellum. Histology demonstrated that most folia lacked granule cells and had randomly misplaced Purkinje cells. Immunohistochemistry revealed the presence of parvoviral antigen in a few neurons and cell processes. PCR targeting feline and canine parvovirus yielded a positive signal. Sequencing analyses from a fragment of the nonstructural protein 1 ( NS1) gene and a portion of the viral capsid protein 2 ( VP2) gene confirmed the presence of DNA of a recent canine parvovirus variant (CPV-2a–like virus) in the cerebellum. Our study provides evidence that (canine) parvovirus may be associated with cerebellar hypoplasia and dysplasia in raccoons, similar to the disease that occurs naturally and has been reproduced experimentally by feline parvoviral infection of pregnant cats, with subsequent intrauterine or neonatal infections of the offspring.


1994 ◽  
Vol 35 (6) ◽  
pp. 1031-1039
Author(s):  
K S Kim ◽  
S Kubota ◽  
M Kuriyama ◽  
J Fujiyama ◽  
I Björkhem ◽  
...  

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 657-668 ◽  
Author(s):  
Randy Mottus ◽  
Richard E Sobel ◽  
Thomas A Grigliatti

Abstract For many years it has been noted that there is a correlation between acetylation of histones and an increase in transcriptional activity. One prediction, based on this correlation, is that hypomorphic or null mutations in histone deacetylase genes should lead to increased levels of histone acetylation and result in increased levels of transcription. It was therefore surprising when it was reported, in both yeast and fruit flies, that mutations that reduced or eliminated a histone deacetylase resulted in transcriptional silencing of genes subject to telomeric and heterochromatic position effect variegation (PEV). Here we report the first mutational analysis of a histone deacetylase in a multicellular eukaryote by examining six new mutations in HDAC1 of Drosophila melanogaster. We observed a suite of phenotypes accompanying the mutations consistent with the notion that HDAC1 acts as a global transcriptional regulator. However, in contrast to recent findings, here we report that specific missense mutations in the structural gene of HDAC1 suppress the silencing of genes subject to PEV. We propose that the missense mutations reported here are acting as antimorphic mutations that “poison” the deacetylase complex and propose a model that accounts for the various phenotypes associated with lesions in the deacetylase locus.


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