Dataset Information

Distribution and genetic diversity of Feline calicivirus in Moscow metropolitan area.

ABSTRACT:

Background

Feline calicivirus (FCV) is widespread throughout the world. An FCV infection is associated with conjunctivitis, rhinitis, and mouth ulcers that can lead to the animal's death. Because vaccination is not always effective, it is necessary to monitor the infection regularly.

Objectives

This study examined the FCV epizootic situation in the Moscow metropolitan area by conducting a molecular phylogenetic analysis of the virus isolates.

Methods

Samples from 6213 animals were examined by a reverse transcription polymerase chain reaction. For phylogenetic analysis, 12 nucleotide sequences obtained from animal samples were selected. Sequencing was performed using the Sanger method. Phylogenetic analysis was conducted using the Maximum Likelihood method.

Results

The FCV genome was detected in 1,596 (25.7%) samples out of 6,213. In 2018, calicivirus was detected in 18.9% of samples, 27.8% in 2019, 21.4% in 2020, and 32.6% in 2021. Phylogenetic analysis of the F ORF2 region and the ORF3 start region led to division into two FCV genogroups. Most of the isolates (8 out of 12) were close to the Chinese strains. On the other hand, there were isolates closely related to European and American strains. The isolates circulating in Moscow were not included in clusters with vaccine strains; their nucleotide similarity varied from 77% to 83%.

Conclusions

This study revealed a high prevalence and genetic diversity of the FCV in Moscow. The epizootic situation remains stably tense because 24 viruses were detected in 25% of animals annually.

SUBMITTER: Komina A

PROVIDER: S-EPMC9715382 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature

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Publications

Distribution and genetic diversity of Feline calicivirus in Moscow metropolitan area.

Komina Alina A Krasnikov Nikita N Kucheruk Oksana O Zhukova Elena E Yuzhakov Anton A Gulyukin Alexey A

Journal of veterinary science 20221101 6

<h4>Background</h4>Feline calicivirus (FCV) is widespread throughout the world. An FCV infection is associated with conjunctivitis, rhinitis, and mouth ulcers that can lead to the animal's death. Because vaccination is not always effective, it is necessary to monitor the infection regularly.<h4>Objectives</h4>This study examined the FCV epizootic situation in the Moscow metropolitan area by conducting a molecular phylogenetic analysis of the virus isolates.<h4>Methods</h4>Samples from 6213 anima ...[more]

PMID: 36448438

Similar Datasets

Project description:Viruses can manipulate the host metabolism to achieve optimal replication conditions, and central carbon metabolism (CCM) pathways are often crucial in determining viral infections. Feline calicivirus (FCV), a diminutive RNA viral agent, induces upper respiratory tract infections in feline hosts, with highly pathogenic strains capable of precipitating systemic infections and subsequent host cell necrosis, thereby presenting a formidable challenge to feline survival and protection. However, the relationship between FCV and host cell central carbon metabolism (CCM) remains unclear, and the precise pathogenic mechanisms of FCV are yet to be elucidated. Upon FCV infection of Crandell-Rees Feline Kidney (CRFK) cells, an enhanced cellular uptake of glucose and glutamine was observed. Metabolomics analyses disclosed pronounced alterations in the central carbon metabolism of the infected cells. FCV infection was found to augment glycolytic activity while sustaining the tricarboxylic acid (TCA) cycle flux, with cellular ATP levels remaining invariant. Concurrently, both glutamine metabolism and the flux of the pentose phosphate pathway (PPP) were noted to be intensified. The application of various inhibitory agents targeting glycolysis, glutamine metabolism, and the PPP resulted in a significant suppression of FCV proliferation. Experiments involving glucose and glutamine deprivation demonstrated that the absence of either nutrient markedly curtailed FCV replication. Collectively, these findings suggest a critical interplay between central carbon metabolism and FCV proliferation. FCV infection stimulates CRFK cells to augment glucose and glutamine uptake, thereby supplying the necessary metabolic substrates and energy for viral replication. During the infection, glutamine emerges as the primary energy substrate, ensuring ATP production and energy homeostasis, while glucose is predominantly channeled into the pentose phosphate pathway to facilitate nucleotide synthesis.

Dataset Information

Distribution and genetic diversity of Feline calicivirus in Moscow metropolitan area.

Background

Objectives

Methods

Results

Conclusions

Publications

Distribution and genetic diversity of Feline calicivirus in Moscow metropolitan area.

Similar Datasets

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