The male reproductive system has a standard immune response regulatory mechanism, However, a variety of external stimuli, including viruses, bacteria, heat, and medications can damage the testicles and cause orchitis and epididymitis. It has been shown that various RNA viruses are more likely to infect the testis than DNA viruses, inducing orchitis and impairing testicular function. It was found that local injection of the viral RNA analog poly(I:C) into the testes markedly disrupted the structure of the seminiferous tubules, accompanied by apoptosis and inflammation. Poly(I:C) mainly inhibited the expression of testosterone synthesis-associated proteins, STAR and MGARP, and affected the synthesis and metabolism of amino acids and lipids in the testis. This led to the disruption of the metabolite levels in the testis of mice, thus affecting the normal spermatogenesis process. The present study analyzed the acute inflammatory response of the testis to viral infection using a multi-omics approach. It provides insights into how RNA virus infection impairs testicular function and offers a theoretical basis for future studies on immune homeostasis and responses under stress conditions in male reproduction.
Keyphrases
- toll like receptor
- nucleic acid
- germ cell
- inflammatory response
- immune response
- oxidative stress
- sars cov
- poor prognosis
- single cell
- amino acid
- liver failure
- endoplasmic reticulum stress
- cell death
- transcription factor
- respiratory failure
- drug induced
- fatty acid
- genetic diversity
- signaling pathway
- adipose tissue
- stress induced
- high fat diet induced
- single molecule
- functional connectivity
- current status
- intensive care unit
- ultrasound guided
- insulin resistance
- skeletal muscle
- resting state
- wild type