Abstract

The evidence for the reverse transcriptase mechanism of somatic hypermutation is substantial and multifactorial. In this 60th anniversary year of the publication of Sir MacFarlane Burnet’s Clonal Selection Theory, the evidence is briefly reviewed and updated.

Highlights

  • The evidence for the reverse transcriptase mechanism of somatic hypermutation is substantial and multifactorial

  • Specialty section: This article was submitted to B Cell Biology, a section of the journal Frontiers in Immunology

  • One reason for writing this Perspective is to counter balance a widely held view in the Ig somatic hypermutation (SHM) field that all relevant studies on the molecular mechanism deal only with the “DNA Deamination Model” which ended in complete consensus over 10 years ago sometime between 2004 and 2007 [Table 1 and Ref. [1] in particular]

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Summary

Introduction

The evidence for the reverse transcriptase mechanism of somatic hypermutation is substantial and multifactorial. The most plausible central molecular mechanism of Ig SHM, that fits with and explains all the evidence [9,10,11] is based on “Reverse Transcription” of the base-modified Ig pre-mRNA (Figure 1).

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