PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of yjbmLink to Publisher's site
 
Yale J Biol Med. 1982 May-Aug; 55(3-4): 193–199.
PMCID: PMC2596440

The clinical illness promotion factor: a third ingredient.

Abstract

The interactions between a causative agent and a susceptible host involve a series of responses most of which are subclinical or asymptomatic but a few of which are manifested by clinical illness. The factor(s) which tip the balance are poorly understood in both acute and chronic diseases. It is designated here as the clinical illness promoting factor (CIPF), a third ingredient. Among infected persons some leads have been found as to why clinical illness develops: in tuberculosis genetic susceptibility plays a key role, as shown in twin studies; in EBV infections age at the time of infection, genetic, and psychosocial factors determine both the expression and the severity of illness; in poliomyelitis age, exercise in the incubation period, and genetic background are related to the development of paralysis. In the relationship between viruses and cancer, viruses and chronic diseases, or inanimate pathogens like tobacco and lung cancer, we know very little as to the factors that result in clinical disease among the many who are presumably susceptible and fully exposed. Epidemiologic study is urged to identify this CIPF or "third ingredient."

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (812K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Evans AS. Causation and disease: the Henle-Koch postulates revisited. Yale J Biol Med. 1976 May;49(2):175–195. [PMC free article] [PubMed]
  • Hallee TJ, Evans AS, Niederman JC, Brooks CM, Voegtly j H. Infectious mononucleosis at the United States Military Academy. A prospective study of a single class over four years. Yale J Biol Med. 1974 Sep;47(3):182–195. [PMC free article] [PubMed]
  • Kasl SV, Evans AS, Niederman JC. Psychosocial risk factors in the developmental of infectious mononucleosis. Psychosom Med. 1979 Oct;41(6):445–466. [PubMed]
  • WILSON MG, SCHWEITZER M. Pattern of hereditary susceptibility in rheumatic fever. Circulation. 1954 Nov;10(5):699–704. [PubMed]
  • Purtilo DT, DeFlorio D, Jr, Hutt LM, Bhawan J, Yang JP, Otto R, Edwards W. Variable phenotypic expression of an X-linked recessive lymphoproliferative syndrome. N Engl J Med. 1977 Nov 17;297(20):1077–1080. [PubMed]
  • de-Thé G, Geser A, Day NE, Tukei PM, Williams EH, Beri DP, Smith PG, Dean AG, Bronkamm GW, Feorino P, et al. Epidemiological evidence for causal relationship between Epstein-Barr virus and Burkitt's lymphoma from Ugandan prospective study. Nature. 1978 Aug 24;274(5673):756–761. [PubMed]
  • Evans AS, Comstock GW. Presence of elevated antibody titres to Epstein-Barr virus before Hodgkin's disease. Lancet. 1981 May 30;1(8231):1183–1186. [PubMed]
  • Ho HC, Kwan HC, Ng MH, de The G. Serum IgA antibodies to Epstein-Barr virus capsid antigen preceding symptoms of nasopharyngeal carcinoma. Lancet. 1978 Feb 25;1(8061):436–436. [PubMed]
  • Lanier AP, Henle W, Bender TR, Henle G, Talbot ML. Epstein-Barr virus-specific antibody titers in seven Alaskan natives before and after diagnosis of nasopharyngeal carcinoma. Int J Cancer. 1980 Aug;26(2):133–137. [PubMed]
  • Yi Z, Yuxi L, Chunren L, Sanwen C, Jihneng W, Jisong Z, Huijong Z. Application of an immunoenzymatic method and an immunoautoradiographic method for a mass survey of nasopharyngeal carcinoma. Intervirology. 1980;13(3):162–168. [PubMed]
  • Gutensohn N, Cole P. Epidemiology of hodgkin's disease in the young. Int J Cancer. 1977 May 15;19(5):595–604. [PubMed]

Articles from The Yale Journal of Biology and Medicine are provided here courtesy of Yale Journal of Biology and Medicine