RNA epitranscriptomics: Regulation of infection of RNA and DNA viruses by N 6 ‐methyladenosine (m 6 A)
Year: 2018
Type: review
Abstract: Summary N 6 ‐methyladenosine (m 6 A) was discovered 4 decades ago. However, the functions of m 6 A and the cellular machinery that regulates its changes have just been revealed in the last few years. m 6 A is an abundant internal mRNA modification on cellular RNA and is implicated in diverse cellular functions. Recent works have demonstrated the presence of m 6 A in the genomes of RNA viruses and transcripts of a DNA virus with either a proviral or antiviral role. Here, we first summarize what is known about the m 6 A “writers,” “erasers,” “readers,” and “antireaders” as well as the role of m 6 A in mRNA metabolism. We then review how the replications of numerous viruses are enhanced and restricted by m 6 A with emphasis on the oncogenic DNA virus, Kaposi sarcoma–associated herpesvirus (KSHV), whose m 6 A epitranscriptome was recently mapped. In the context of KSHV, m 6 A and the reader protein YTHDF2 acts as an antiviral mechanism during viral lytic replication. During viral latency, KSHV alters m 6 A on genes that are implicated in cellular transformation and viral latency. Lastly, we discuss future studies that are important to further delineate the functions of m 6 A in KSHV latent and lytic replication and KSHV‐induced oncogenesis.
Source: Reviews in Medical Virology
DOI: 10.1002/rmv.1983
Authors: Brandon Tan, Shou‐Jiang Gao
Language: English
Topic: RNA modifications and cancer
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
Awards: Targeting KSHV malignancies and persistent infection, HISTONE MODIFIERS IN ORAL KSHV INFECTION AND MALIGNANCIES, KSHV microRNAs in tumor invasion and angiogenesis, Mechanism of KSHV-induced angiogenesis, KSHV microRNAs in cellular transformation and tumorigenesis, Regulation of KSHV replication by N6-methyladenosine (m6A), Cell model for KSHV infection and genetic manipulation
OpenAlex ID: W2803000225