Literature DB >> 17509771

Keloids: A viral hypothesis.

Pedro E Alonso1, Luis F Rioja, Carlos Pera.   

Abstract

The triggering cause of keloid formation on a healing wound remains an enigma. In fact, the hypotheses put forward so far to explain this phenomenon seem inconsistent with some clinical features of the disease. The recently established bonds between infectious agents and some pathologies of unknown origin such as peptic ulcer disease, Kaposi's sarcoma or cervical cancer among others led us to consider a potential infectious origin for keloids. This paper presents an infection-based hypothesis (specifically, a viral hypothesis) intended to account for most of their clinical features. Essentially, we hypothesize that healthy individuals carrying a virus, whether known or unknown, associated to some adjuvant, and having some genetic susceptibility, may develop keloids during the scar maturation process in the following manner: the virus would make the bone marrow or lymphatic system its reservoir, residing there in a silent state, and reach the wound via two different mechanisms. The primary mechanism might use an internal circuit through which the viral genome would be transported from its myeloid reservoir to the wound via bone marrow or circulating fibrocytes chemotactically attracted to the damaged skin region. The secondary mechanism might involve an external circuit by which infecting virions via saliva would be shed in the wound directly (preferentially in the sternal or deltoid region) or indirectly (other satellite regions) via the hands or some fomites. A combination of both mechanisms might also be possible. Once in the wound, the virus would switch from a silent state to a latent state by effect of some chemical stimulus probably generated during the tissue repair process; in the new state, the transcription of some of the powerful viral proteins might cause thorough derailment of the normal repair process. As a result, keloid growth might depend both on individual susceptibility and on the viral load deposited into the wound; the greater the susceptibility and viral load were, the more markedly the keloid would develop and the more aggressive it would be.

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Year:  2007        PMID: 17509771     DOI: 10.1016/j.mehy.2007.03.023

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  4 in total

1.  Upregulation of proinflammatory genes in skin lesions may be the cause of keloid formation (Review).

Authors:  Xianglin Dong; Shaolin Mao; Hao Wen
Journal:  Biomed Rep       Date:  2013-09-25

Review 2.  New approach to the understanding of keloid: psychoneuroimmune-endocrine aspects.

Authors:  Bernardo Hochman; Felipe Contoli Isoldi; Fabianne Furtado; Lydia Masako Ferreira
Journal:  Clin Cosmet Investig Dermatol       Date:  2015-02-10

3.  The 1470 nm diode laser with an intralesional fiber device: a proposed solution for the treatment of inflamed and infected keloids.

Authors:  Ke Li; Fabio Nicoli; Wen Jing Xi; Zheng Zhang; Chunxiao Cui; Ahmed Al-Mousawi; Alberto Balzani; Yun Tong; Yixin Zhang
Journal:  Burns Trauma       Date:  2019-02-15

Review 4.  The Keloid Disorder: Heterogeneity, Histopathology, Mechanisms and Models.

Authors:  Grace C Limandjaja; Frank B Niessen; Rik J Scheper; Susan Gibbs
Journal:  Front Cell Dev Biol       Date:  2020-05-26
  4 in total

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