Contagious obesity: from adenovirus 36 to RB dysfunction

TL;DR

This paper explores the hypothesis that adenovirus 36 may contribute to obesity by inactivating the RB protein, offering new perspectives on infectious causes and potential intervention strategies for obesity.

Contribution

It proposes a novel mechanism linking adenovirus 36 to obesity through RB protein inactivation, expanding understanding of infectious factors in obesity.

Findings

Adenovirus 36 may inactivate RB protein, influencing obesity development.

Inactivation mechanism resembles that of other adenoviruses and insulin.

Suggests new intervention approaches targeting viral interactions with RB.

Abstract

Significant overweight represents a major health problem in industrialized countries. Besides its known metabolic origins, this condition may also have an infectious cause, as recently postulated. Here, it is surmised that the potentially causative adenovirus 36 contributes to such disorder by inactivating the retinoblastoma tumor suppressor protein (RB) in a manner reminiscent of a mechanism employed by both another pathogenic adenoviral agent and insulin. The present insight additionally suggests novel modes of interfering with obesity-associated pathology.