FC 23-08Is the persisting HPV genotype on anal swab the causative genotype in HGAIN lesions?

25. Anal neoplasia
A. Leeman 1, E. Marra 2, M.L. Siegenbeek Van Heukelom 3, M.M. Van De Sandt 1, D. Jenkins 1, H.C.J. De Vries 4, A. Van Eeden 5, J.M. Prins 3, C.J. Meijer 6, W.G.V. Quint 1, M.F. Schim Van De Loeff 7.
1DDL Diagnostic Laboratory, Visseringlaan 25, 2288 ER Rijswijk (Netherlands), 2Public Health Service of Amsterdam, Department of Infectious Diseases, P.O. Box 2200, 1000CE, Amsterdam, (Netherlands), 3Academic Medical Center, Department of Infectious Diseases, University of Amsterdam, P.O. Box 22700, 1100DE, Amsterdam (Netherlands), 4Academic Medical Center, Department of Dermatology, University of Amsterdam, P.O. Box 22700, 1100DE, Amsterdam (Netherlands), 5DC Klinieken, Amsterdam (Netherlands), 6Department of Pathology, VU University Medical Centre, Amsterdam (Netherlands), 7Public Health Service of Amsterdam, Department of Infectious Diseases, P.O. Box 2200, 1000CE, Amsterdam (Netherlands)

Background / Objectives

To study the correlation between persistent type-specific HPV infection on anal swabs and the causative HPV type in HGAIN lesions in HIV+ MSM.


Methods

A cohort of HIV+ MSM was followed for two years with 6-monthly anal swabs. Swabs were tested for HPV DNA and typed using the SPF10-PCR-DEIA-LiPA25v1 system. Men in whom at least 4/5 anal swabs were positive for the same HPV type were considered to have a persistent anal HPV infection. After this 24-month period men were assessed by High Resolution Anoscopy (HRA), and biopsies were taken. For the present analysis, we selected MSM with persisting anal HPV infections on swab and HGAIN on histology (N=30). After reviewing of HE and p16 slides for the worst diagnosis (AIN2 or AIN3), worst lesions collected using laser capture microdissection were tested for HPV with the same system which resulted in identification of the causative genotypes. We assessed the correlation between persistent type-specific HPV infection on swab and the causative HPV type of HGAIN lesions. 


Results

After exclusion of 5 patients in whom the worst diagnosis upon re-examination was less than HGAIN, 51 biopsies from 25 men remained. Worst lesion found on patient level was AIN2 in 9 men and AIN3 in 16 men. On the anal swabs, 12 men had persisting HPV infection of a single HPV genotype (3 lrHPV, 9 hrHPV), and 13 with multiple types. Of the men with multiple persisting HPV genotypes, one man had lrHPV genotypes only, 4 had hrHPV genotypes only and 8 had both lrHPV and hrHPV genotypes. HPV6 was the most frequently found persisting genotype (36%). On biopsy, four men had (multiple) HGAIN lesions with different HPV genotypes and 21 men had one HGAIN lesion with a single causative HPV genotype. The most frequently found genotype in HGAIN lesions was HPV 16 (28%, 7/25). The causative HPV type (1 lrHPV and 24hrHPV) was the same as the persisting type in 11/25 (44%) men with HGAIN: 2/9 (22%) in AIN2 and 9/16 (56%) in AIN3. In 8/25 men (32%) the causative type was not persistent, but was detected in at least one of the swabs. In 6/25 men the causative type was never found in anal swabs (24%). 


Conclusion

A persisting genotype was marked as a causative genotype in only 44% of the men with a HGAIN lesion, with a remarkable difference in correlation with AIN2 (22%) and AIN3 (56%). In 32%, the causative genotype was detected in at least one of the swabs and in 24% the causative genotype was never detected on swab in the 2 years prior to HRA. These results demonstrate that the causative genotype is often not persistently or not detected on swabs. Therefore, serial anal swabs may have limited value in screening for HGAIN, but AIN3 is linked to persistence more often than AIN2.


References