Marek's Disease Virus Infection Induced Mitochondria Changes in Chickens.
Qin ChuYi DingWentao CaiLei LiuHuanmin ZhangJiuzhou SongPublished in: International journal of molecular sciences (2019)
Mitochondria are crucial cellular organelles in eukaryotes and participate in many cell processes including immune response, growth development, and tumorigenesis. Marek's disease (MD), caused by an avian alpha-herpesvirus Marek's disease virus (MDV), is characterized with lymphomas and immunosuppression. In this research, we hypothesize that mitochondria may play roles in response to MDV infection. To test it, mitochondrial DNA (mtDNA) abundance and gene expression in immune organs were examined in two well-defined and highly inbred lines of chickens, the MD-susceptible line 72 and the MD-resistant line 63. We found that mitochondrial DNA contents decreased significantly at the transformation phase in spleen of the MD-susceptible line 72 birds in contrast to the MD-resistant line 63. The mtDNA-genes and the nucleus-genes relevant to mtDNA maintenance and transcription, however, were significantly up-regulated. Interestingly, we found that POLG2 might play a potential role that led to the imbalance of mtDNA copy number and gene expression alteration. MDV infection induced imbalance of mitochondrial contents and gene expression, demonstrating the indispensability of mitochondria in virus-induced cell transformation and subsequent lymphoma formation, such as MD development in chicken. This is the first report on relationship between virus infection and mitochondria in chicken, which provides important insights into the understanding on pathogenesis and tumorigenesis due to viral infection.
Keyphrases
- mitochondrial dna
- copy number
- gene expression
- genome wide
- dna methylation
- disease virus
- molecular dynamics
- cell death
- high glucose
- immune response
- reactive oxygen species
- diabetic rats
- endoplasmic reticulum
- drug induced
- single cell
- stem cells
- magnetic resonance
- cell therapy
- heat stress
- toll like receptor
- bioinformatics analysis
- dendritic cells
- transcription factor
- microbial community
- inflammatory response
- bone marrow