TY - JOUR
T1 - Epstein-barr virus BBRF2 is required for maximum infectivity
AU - Al Masud, H. M.Abdullah
AU - Yanagi, Yusuke
AU - Watanabe, Takahiro
AU - Sato, Yoshitaka
AU - Kimura, Hiroshi
AU - Murata, Takayuki
N1 - Funding Information:
This work was supported by grants-in-aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology (to T.M. (19K07580) and H.K. (17H04081)), Japan Agency for Medical Research and Development (to T.M. (Japanese Initiative for Progress of Research on Infectious Disease for Global Epidemic, JP17fm0208016) and H.K. (Practical Research Project for Rare/Intractable Diseases, JP16ek0109098)), the Takeda Science Foundation (to T.M.), and the Hori Sciences and Arts Foundation (to T.M. and H.K.). We thank W. Hammerschmidt, H. J. Delecluse, T. Kanda, H. Yoshiyama, F. Goshima, and T. Tsurumi for materials and discussions.
PY - 2019/12
Y1 - 2019/12
N2 - Epstein-Barr virus (EBV) is a member of the gammaherpesvirinae, which causes infectious mononucleosis and several types of cancer. BBRF2 is an uncharacterized gene of EBV and is expressed during the lytic phase. To evaluate its function, BBRF2-knockout EBV was prepared using bacterial artificial chromosome (BAC) technology and the CRISPR/Cas9 system. Although viral gene expression, DNA synthesis, and progeny secretion were not affected, the infectivity of progeny viruses was significantly reduced by the disruption of BBRF2. When expressed alone, BBRF2 protein localized to the nucleus and cytoplasm, while the coexpression of an interacting partner, BSRF1, resulted in its relocalization to the cytoplasm. Interestingly, the coexpression of BBRF2 protected BSRF1 from proteasome/ubiquitin-dependent degradation. Therefore, BBRF2, together with BSRF1, augments viral infectivity.
AB - Epstein-Barr virus (EBV) is a member of the gammaherpesvirinae, which causes infectious mononucleosis and several types of cancer. BBRF2 is an uncharacterized gene of EBV and is expressed during the lytic phase. To evaluate its function, BBRF2-knockout EBV was prepared using bacterial artificial chromosome (BAC) technology and the CRISPR/Cas9 system. Although viral gene expression, DNA synthesis, and progeny secretion were not affected, the infectivity of progeny viruses was significantly reduced by the disruption of BBRF2. When expressed alone, BBRF2 protein localized to the nucleus and cytoplasm, while the coexpression of an interacting partner, BSRF1, resulted in its relocalization to the cytoplasm. Interestingly, the coexpression of BBRF2 protected BSRF1 from proteasome/ubiquitin-dependent degradation. Therefore, BBRF2, together with BSRF1, augments viral infectivity.
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U2 - 10.3390/microorganisms7120705
DO - 10.3390/microorganisms7120705
M3 - Article
AN - SCOPUS:85076765443
VL - 7
JO - Microorganisms
JF - Microorganisms
SN - 2076-2607
IS - 12
M1 - 705
ER -