Key result
REV infection initially increases then decreases splenic TRIM62 expression, suggesting it inhibits antiviral activity.
Why the study?
Although chicken TRIM62 was shown to inhibit REV replication, the effect of viral infection on the distribution of TRIM62 remained unknown.
REV infection appears to inhibit the antiviral activity of TRIM62 by decreasing its expression, particularly in the spleen.
REV may inhibit TRIM62 antiviral activity in avian spleen; hypothesis-generating for retroviral evasion mechanisms.
The tripartite motif containing 62 (TRIM62) is a host antiviral factor. It was demonstrated in our previous study that chicken TRIM62 significantly inhibited the replication of reticuloendotheliosisvirus (REV). However, the effect of viral infection on the distribution of TRIM62 is still unknown. In the present study, we tested and evaluated the tissue distribution of TRIM62 and the REV infection correlativity. We found that the distribution and mRNA expression of TRIM62 were first increased and then decreased upon REV infection. The decrease of TRIM62 was mostly in the spleen. The results suggest REV inhibited the antiviral activity of TRIM62 by decreasing its expression.
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Yang et al. (2020) studied Reticuloendotheliosisvirus (REV) infection. REV infection was evaluated on Distribution and mRNA expression of TRIM62. REV infection initially increased and then decreased the distribution and mRNA expression of TRIM62, mostly in the spleen, suggesting REV inhibits TRIM62 antiviral activity.
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