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ntm4-30-7 Mad rantings about politics, evolution, and microbiology. Comment policy: say what you want, but back it up with an email address. I don't like anonymous trolls.

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A Cancer-Causing Virus...Protects Against Cancer?

Posted on: June 26, 2008 11:06 AM, by Mike

In a Journal of Infectious Diseases commentary about this article, there's a fascinating discussion of the relationship between the HTLV-1 virus, which can cause T-cell leukemia in about one percent of those infected, and gastric cancer caused by the bacterium Helicobacter pylori. And it's not what you would expect.

Here's the summary (italics mine; references removed for clarity):

In this issue of the Journal, Matsumoto et al. asked whether human T lymphotropic virus type 1 (HTLV-1) antibody status is associated with the risk of developing gastric cancer. In a cohort of >5000 patients aged >40 years who were enrolled during 1989-1992 in an HTLV-1-endemic area, they identified 1812 subjects who underwent endoscopy of the upper gastrointestinal tract before 2003. Of those who were free of gastric cancer on that examination, 497 HTLV-1 antibody positive patients were selected and matched with 497 control patients who were HTLV-1 antibody negative. Both groups were followed for 9.5 years to determine who would develop gastric cancer. The major finding of the study was that gastric cancer developed less frequently among HTLV-1-positive subjects than among HTLV-1-negative subjects (2.8% vs. 7.0%). The findings are convincing because no sources of differential bias were obvious, the results confirm and are similar to those of a previous study, the time courses in Kaplan-Meier analysis are internally consistent, and the results for men and women were parallel with similar levels of inverse association (odds ratio, 0.38). Thus, the inverse association between HTLV-1 infection and development of gastric cancer that was uncovered in this prospective study should be considered correct.

That's right: a virus that occasionally results in leukemia protects you from gastric cancer. While the mechanism is unclear, the result appears solid. What's even more interesting is that this mutualism* may be disappearing due to changes in human behavior:

What are the implications of finding an interaction between HTLV-1 and H. pylori? Both microbes are rapidly disappearing because of public health measures (in the case of HTLV-1) and because of changes extant in modern life, possibly driven by antibiotic use (in the case of H. pylori). As such, the epidemiologic significance of the interaction between these 2 microbes may lessen over time. Nevertheless, the linkage has important implications in human cancer biology. The concept of a protective effect suggests that HTLV-1 may be a form of viral commensal of humans, protecting hosts through interference with H. pylori-induced pathology.

Really cool stuff.

*While the authors call this a commensalism, I think mutualism is the appropriate term, as both organisms gain.

Cited articles: Matsumoto, S., K. Yamasaki, K. Tsuji, & S. Shirahama. 2008. Human T Lymphotropic Virus Type 1 Infection and Gastric Cancer Development in Japan. The Journal of Infectious Diseases 198:10-15.

Blaser, M.J., & F.T. Valentine. 2008. Viral Commensalism in Humans? The Journal of Infectious Diseases 198:1-3
.

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Comments

1

Way cool. Wonder if there are similar brakes on HIV, by HEP C, or similar, Chris

Posted by: Chris | June 26, 2008 12:33 PM

2

Ahhgh include the CI in the OR people, please!
Ok, so I must go read the whole thing. To me, this actually isn't suprising. I was just commenting the other day that the relationship between cancer and inflammmation is really complicated. Too much growth of T-cells helps get the microbe population down but puts you at a risk of T-cell cancer. Too little growth of T-cells and the microbes sit in your stomach for years, causing inflammation. This results in reactive oxygen species damaging the epithelial cells' DNA, leading to cancer. OK, so it's not a specific mechanism yet, but it does make sense in a broad sense.

VERY COOL.

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