Do some viruses use growth hormone, prolactin and their receptors to facilitate entry into cells?

Abstract

The molecular evolution of pituitary growth hormone and prolactin in mammals shows two unusual features: episodes of markedly accelerated evolution and, in some species, complex families of related proteins expressed in placenta and resulting from multiple gene duplications. Explanations of these phenomena in terms of physiological adaptations seem unconvincing. Here, I propose an alternative explanation, namely that these evolutionary features reflect the use of the hormones (and their receptors) as viral receptors. Episodes of rapid evolution can then be explained as due to “arms races” in which changes in the hormone lead to reduced interaction with the virus, and subsequent changes in the virus counteract this. Placental paralogues of the hormones could provide decoys that bind viruses, and protect the foetus against infection. The hypothesis implies that the extensive changes introduced into growth hormone, prolactin and their receptors during the course of mammalian evolution reflect viral interactions, not endocrine adaptations.

The crucial role of prolactin-lactogenic hormone in Covid-19

“…Accordingly, Wallis in 2021 demonstrated that CMV and other viruses like rubella can use PRLRs as receptor and entry point for viral-host cell interactions [55]. In SARS epidemic 2003, SARS-CoV led to significant increase in PRL serum level due to dysregulation of adenohypophyseal control by direct cytopathic effect or associated pro-inflammatory changes [56].…”

dPRLR causes differences in immune responses between early and late feathering chickens after ALV-J infection

“…Receptors for growth factors, cytokines or hormones are clearly potential viral receptors, as they are already adapted to bind to specific circulating ligands and subsequently promote viral entry and survival by receptor-mediated endocytosis [ 34 ]. The receptors known to be used by viruses include insulin-like growth factor 1 receptor (IGF1R), platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) [ 35 , 36 ].…”

dPRLR Cause the Differences in Immune Responses Between Early and Late Feathered Chickens After ALV-J Infection

“…Receptors for growth factors, cytokines or hormones are clearly potential targets as viral receptors in that they are already adapted to bind to speci c circulating ligands, and subsequently promote viral entry and survival by receptor-mediated endocytosis [34]. Receptors known to be used by viruses include insulin-like growth factor 1 receptor (IGF1R), platelet derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) [35,36].…”