On 2016 Apr 28, Donald Forsdyke commented:

RNAS ENCODING HBZ AND EBNA1 PROTEINS ARE BOTH PURINE-LOADED

The sensitive quantification of HBZ protein levels in various clinical conditions (1) is a major advance. Unlike other HTLV1 proteins, the latency-controlling HBZ protein is encoded by the antisense strand. Thus, whereas the main-gene-encoding ‘top’ strand of the latent virus is pyrimidine-rich, the complementary, ‘bottom,’ strand that encodes HBZ is purine-rich. Likewise, most genes in Epstein-Barr virus are encoded by pyrimidine-rich strands, but the latency-controlling EBNA1 protein is encoded by a purine-rich strand.

The speculation that this purine-loading militates against the formation of double-stranded RNA and hence dampens the host immune response (2) is in keeping with:

(a) the “extremely low expression and immunogenicity of HBZ in natural HTLV-1 infection,”

(b) the possibility that “the most important actions of HBZ, which are critical to HTLV-1 persistence, are exerted at the RNA level, and not the protein level,” and

(c) the view that “minimized HBZ protein translation is a sophisticated viral strategy for evasion from the host T cell response.”

(1) Shiohama et al. (2016) Retrovirology 13:29 Shiohama Y, 2016

(2) Forsdyke DR (2014) Microbes and Infection 16, 96-103 Forsdyke DR, 2014

On 2016 Apr 28, Donald Forsdyke commented:

RNAS ENCODING HBZ AND EBNA1 PROTEINS ARE BOTH PURINE-LOADED

The sensitive quantification of HBZ protein levels in various clinical conditions (1) is a major advance. Unlike other HTLV1 proteins, the latency-controlling HBZ protein is encoded by the antisense strand. Thus, whereas the main-gene-encoding ‘top’ strand of the latent virus is pyrimidine-rich, the complementary, ‘bottom,’ strand that encodes HBZ is purine-rich. Likewise, most genes in Epstein-Barr virus are encoded by pyrimidine-rich strands, but the latency-controlling EBNA1 protein is encoded by a purine-rich strand.

The speculation that this purine-loading militates against the formation of double-stranded RNA and hence dampens the host immune response (2) is in keeping with:

(a) the “extremely low expression and immunogenicity of HBZ in natural HTLV-1 infection,”

(b) the possibility that “the most important actions of HBZ, which are critical to HTLV-1 persistence, are exerted at the RNA level, and not the protein level,” and

(c) the view that “minimized HBZ protein translation is a sophisticated viral strategy for evasion from the host T cell response.”

(1) Shiohama et al. (2016) Retrovirology 13:29 Shiohama Y, 2016

(2) Forsdyke DR (2014) Microbes and Infection 16, 96-103 Forsdyke DR, 2014