35

CASE 35


CW is a 30-year-old woman in your practice whose recent annual “Pap” smear results have just come to your attention. The diagnosis reads CIN type II (CIN = cervical intraepithelial neoplasia), which indicates inflammatory change and abnormal preneoplastic cells. You arrange a biopsy for her with your referring gynecologist, who confirms this result. In the meantime you order a serologic study for measurement of human papillomavirus 16 (HPV-16) antibody titers and a cervicovaginal lavage specimen to test for the presence of HPV-16 DNA. HPV-16 is implicated as a causative agent in cervical cancer. Based on recent findings in the literature, you wonder whether this woman could be considered for HPV-16 immunization. What other recommendations should you make?



QUESTIONS FOR GROUP DISCUSSION



1. What is a “Pap” smear?

2. Human papillomavirus is transmitted sexually. Most infections are benign, despite the fact that there are more than 50 types that can infect the genitalia. Which type has been isolated from over 50% of cancers of the cervix?

3. Explain why a serologic test is performed even though it is not diagnostic for a present infection.

4. What is the rationale for performing a DNA test for HPV-16? Why is an amplification test (e.g., polymerase chain reaction [PCR]) more likely to detect HPV than other types of DNA tests?

5. What is the generally accepted form of treatment for a CIN type II?

6. Where does the immunogenicity of papillomaviruses reside?

7. Explain how “empty viral capsids” are generated and why they have been considered as potential vaccines for women at high risk for cervical malignancy.

8. Discuss the results of a double-blind randomized study using this vaccine.

9. How would you advise the women in the study who experienced seroconversion but who did not have any evidence for cervical changes?

10. Explain the role of the HPV transformation proteins E6 and E7.


RECOMMENDED APPROACH



Implications/Analysis of Family History


No family history is provided and this is not particularly relevant at this time. Although there are a number of non-HPV factors that contribute to subsequent malignancy, among them being genetic predisposition, the particular contributing gene has not been identified. One could speculate that genetic alterations in any one of a number of immune components could impact on the individual’s ability to eliminate viral infections and hence susceptibility to progression to malignancy. However, at this time, these are not well enough defined to be included in the assessment of the patient.



Implications/Analysis of Clinical History

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Jun 18, 2016 | Posted by in IMMUNOLOGY | Comments Off on 35

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