Human herpes virus8 (HHV-8) is a known carcinogenic agent. This report investigates five populations to determine if HHV-8 was associated with disease onset. Detection and levels of antibodies were measured using an enhanced immunofluorescent assay and were analyzed with the statistical program, SPSS.
In the first study, we tested the hypothesis that HHV-8 was the causative agent in Langerhans cell histiocytosis (LCH). The seroprevalence of HHV-8 among 159 LCH patients was similar to the control group, indicating that HHV-8 is not the etiological agent of LCH.
In the second study, we tested the hypothesis that HHV-8 reactivation occurs in solid-organ transplant (SOT) patients, following immunosuppression. We found a significant increase in HHV-8 seropositivity when comparing pre-transplant to post-transplant samples (p-less than .01). There was also an overall increase in viral antibody titers following transplantation (p=less than .001), indicating viral reactivation. In the third study, we compare the SOT results to bone-marrow transplant patients (BMT). Longitudinal serum samples from 34 BMT patients did not demonstrate a significant association with HHV-8 as compared to the control (p=.716) or the SOT populations (p=.180). In addition, HHV-8 reactivation did not occur post-transplantation.
In the fourth study, we tested the hypothesis that HHV-8 is associated with increased risk of prostate cancer (PrCa). There was greater than a 2-fold association between HHV-8 seroprevalence and PrCa among African-Caribbean men from Tobago (p=.003). A similar trend was present in a PrCa cohort from the United States, p=greater than .05.
In a fifth study, we tested the hypothesis that HHV-8 increased the risk of PrCa among men who carried genetic polymorphisms in the androgen (AR) and estrogen receptor (ESR1) genes. This study analyzed an expanded Tobago cohort, which demonstrated an association between HHV-8 and PrCa (OR 1.74, p=.032). An increased association was found among seropositive men carrying the high-risk AR allele (OR=2.46, p=.023) and ESR1 allele (OR=3.10, p=.004). The strongest association was found in seropositive men with both high-risk alleles (OR=5.20, p=.017).
This study demonstrates the use of HHV-8 serology as a marker for an increased public health cancer detectable risk, due to viral prevalence or reactivation.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-04132005-195044 |
| Date | 09 June 2005 |
| Creators | Hoffman, Linda J. |
| Contributors | Charles R. Rinaldo, Ph.D., Clareann H. Bunker, Ph.D., Christine Milcarek, Ph.D., Frank J. Jenkins, Ph.D. |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-04132005-195044/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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