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Feng Wen

Publications and source records attributed to Feng Wen.

2 recordsLinked to original sources
PubMed2026

The prevalence and molecular characterization of Porcine teschoviruses in Guangdong Province, China.

Porcine teschoviruses (PTVs) are globally endemic and widely circulate within pig populations. This study aimed to investigate the prevalence and genetic characteristics of PTVs in Guangdong Province, China. A total of 341 fecal and 99 tissue mixture samples were collected from pigs in seven cities across the province. These samples were screened for PTVs using reverse transcription-polymerase chain reaction (RT-PCR). The overall PTV positivity rate was determined to be 19.32%. In this study, the PTV3 PTV/CN/GD/316 strain was successfully isolated from a tissue mixture sample obtained from a pig exhibiting diarrhea. The isolation was performed using swine testicular (ST) cells. The complete viral genome of this isolate measured 6,999 nucleotides (nt) and encoded a polyprotein of 2,205 amino acids. Phylogenetic analysis of the complete VP1 gene identified seven distinct PTV genotypes (PTV2, PTV3, PTV4, PTV9, PTV14, PTV17, and PTV19) among the 21 PTV isolates obtained, with PTV3 being the dominant genotype (38.10%), followed by PTV9 (19.05%). Furthermore, our findings revealed a significant co-infection of PTVs with other common swine pathogens, including PCV2, PEDV, PCV3, PRRSV, CSFV, and PDCoV. The co-infection rate with these viruses was remarkably high, reaching 97.65%. Collectively, these data demonstrate the widespread circulation of PTVs in pig farms in Guangdong Province and highlight the prevalence of co-infection scenarios with other viral agents. The genetic analyses of all available PTV VP1 sequences also underscore the considerable diversity of PTV genotypes circulating within the Guangdong region.IMPORTANCECurrently, PTVs are widespread globally, with their infection rates showing a rising trend. The prevalence and molecular characterization of PTVs help prevent and control the spread of diseases. The findings of this study indicate a high prevalence and considerable genetic diversity of PTVs in certain areas of Guangdong Province, China. The occurrence of co-infection with other pathogens is also relatively common. Based on these data, we can better safeguard swine health and mitigate the economic impact of these infections on the agricultural industry.

Guangdong Province↗
PubMed2010

Mouse Prkar1a haploinsufficiency leads to an increase in tumors in the Trp53+/- or Rb1+/- backgrounds and chemically induced skin papillomas by dysregulation of the cell cycle and Wnt signaling.

PRKAR1A inactivation leads to dysregulated cAMP signaling and Carney complex (CNC) in humans, a syndrome associated with skin, endocrine and other tumors. The CNC phenotype is not easily explained by the ubiquitous cAMP signaling defect; furthermore, Prkar1a(+/-) mice did not develop skin and other CNC tumors. To identify whether a Prkar1a defect is truly a generic but weak tumorigenic signal that depends on tissue-specific or other factors, we investigated Prkar1a(+/-) mice when bred within the Rb1(+/-) or Trp53(+/-) backgrounds, or treated with a two-step skin carcinogenesis protocol. Prkar1a(+/-) Trp53(+/-) mice developed more sarcomas than Trp53(+/-) mice (P < 0.05) and Prkar1a(+/-) Rb1(+/-) mice grew more (and larger) pituitary and thyroid tumors than Rb1(+/-) mice. All mice with double heterozygosity had significantly reduced life-spans compared with their single-heterozygous counterparts. Prkar1a(+/-) mice also developed more papillomas than wild-type animals. A whole-genome transcriptome profiling of tumors produced by all three models identified Wnt signaling as the main pathway activated by abnormal cAMP signaling, along with cell cycle abnormalities; all changes were confirmed by qRT-PCR array and immunohistochemistry. siRNA down-regulation of Ctnnb1, E2f1 or Cdk4 inhibited proliferation of human adrenal cells bearing a PRKAR1A-inactivating mutation and Prkar1a(+/-) mouse embryonic fibroblasts and arrested both cell lines at the G0/G1 phase of the cell cycle. In conclusion, Prkar1a haploinsufficiency is a relatively weak tumorigenic signal that can act synergistically with other tumor suppressor gene defects or chemicals to induce tumors, mostly through Wnt-signaling activation and cell cycle dysregulation, consistent with studies in human neoplasms carrying PRKAR1A defects.

Animals↗