Research from the University of California, Irvine has revealed how a protein, APOBEC3B, could protect cells against different types of RNA viruses, helping to prevent disease. 

Findings from the study, published in Nature Communications, provide an understanding of how lung cells, in particular, protect themselves against RNA viral infection. The discovery is essential to developing future therapies to limit viral infection and improve the health of patients with chronic lung disease, according to a press release from the University of California, Irvine. 

Respiratory syncytial virus, SARS-CoV2, influenza, poliovirus, and measles—all single-stranded RNA viruses—are some examples of highly contagious diseases transmitted by respiratory aerosols that commonly infect lung cells.

“Patients with chronic lung diseases, such as asthma, cystic fibrosis, chronic obstructive pulmonary disease, and interstitial lung diseases, are more susceptible to respiratory lung infections. These viral infections can further contribute to disease progression,” says Remi Buisson, PhD, assistant professor at the University of California, Irvine School of Medicine Department of Biological Chemistry, in a press release. “An exciting part of our finding fills a critical knowledge gap by illuminating how APOBEC3B can promote innate immune responses in host cells without generating mutations in the virus genomes and promoting viral evolution.”

In this study, graduate students Lavanya Manjunath and Sunwoo Oh, both at the University of California, Irvine School of Medicine in the Buisson Laboratory, utilized different RNA virus models, including Sendai virus, poliovirus, and Sindbis virus, as tools to determine how APOBEC3B regulates innate immune signaling in response to viral infection. 

Moreover, they found that APOBEC3B is recruited to stress granules through its interaction with PABPC1 to prevent stress granule destabilization and protect mRNAs associated with stress granules from an RNA endonuclease RNase L that cleave RNAs in host cells.

“We propose that APOBEC3B, in addition to its canonical role to edit viral genomes, functions with PABPC1 as important innate immunity mediators, protecting cells at different steps of the innate immune response against viral infections,” says Buisson in a press release. 

More research is needed to develop strategies to prevent RNA viral infection. Researchers say the next step is to determine how APOBEC3B recognizes viral genome to promote an innate immune response and prevent viral replication, with a goal of identifying how RNA viruses developed resistance mechanisms to counteract APOBEC3B functions and escape host cell defense.