Epigenetics and Virus

Latest World Health Organization data show that the Ebola virus have take away the lives of 887 people in 4 African countries, the cumulative number of reported cases has reached to more than 1600. The virus quickly breaks the human immune system, and ravage in the African region. Ebola virus is a kind of infectious disease virus, which can make humans and primates have Ebora fever, and result in a high mortality rate of between 50% and 90%, the main cause of death is the stroke, myocardial infarction, hypovolemic shock and multiple organ failure.

Fortunately, to prevent the spread of the deadly Ebola virus, clinical trials for Ebola vaccine will be accelerated, and is expected to be widely applied next year. Perhaps the study on the epigenetic and virus may give us some different implications for the therapy of Ebola virus disease.

Viruses are known to propagate using host transcription and translation system, and some virus genomes are organized into chromatin-like structure, which undergoes different histone modifications facilitating complex functions in virus life cycles including replication. Also, some viruses actively modulate cellular epigenetic factors to survive and propagate in host cells. Thus, relationship between epigenetics and virus is worth studying.

According to the previous study results, virus replication can be regulated by various epigenetic mechanisms, including histone acetylation, DNA methylation, nucleosome remodeling, and miRNA.

Some active histone marks such as histone H3/H4 acetylation and H3K4me3 in viral regulatory regions will be enriched when viral gene activation and reactivation from latency happen, while those negative histone markers such as H3K9me, H3K27me3, and H4K20me3 are always accompanied with chromatin repression and latency maintenance. For example, EBV canbe reactivated after knockdown or inhibition of the activity of EZH2 and SUV420H1, which are HMTs for H3K27me3 and H4K20me3, respectively.

After infection, viruses also regulate host gene expression by altering histone modifications and chromatin structure in order to survive and replicate in host. For example, KSHV vIRF represses the expression of a cellular cytokine (MIF) to circumvent IFN-mediated host defense immune response by preventing its histone acetylation. HPV16 also can reduce TLR9 expression and attenuate interferon response by recruiting HDAC1 and histone demethylase to TLR9 promoter to reduce H4 acetylation and H3K4me3.

Thus, it is critical for exploring the new therapy for virus diseases to understand how virus infection causes epigenetic changes and how viruses utilize the host epigenetic machinery to accommodate their infection.

Numerologist Warda is hooked on OG-L002 fishing, collecting. And lastly her encouragement comes from socializing along with her companions.