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The clearance of B19 parvovirus from peripheral blood was followed after acute infection to determine how long the virus is present in blood, even at low titer. The presence of B19 DNA in serum was investigated with dot blot hybridization during an epidemic. Fourteen patients positive for B19 DNA were followed for up to 1 year for its presence in samples taken monthly, using both dot blot hybridization and nested polymerase chain reaction (PCR). All patients examined showed medium to high viremic titers (detectable with hybridization assay) only at the beginning of observation; later the virus titer decreased and was detectable only by nested PCR. Of the 14 patients followed, 13 were positive for B19 DNA by nested PCR for 2-6 months; 1 patient showed a persistent infection associated with chronic arthritis and was positive for B19 DNA for 1 year without clearance of the virus.

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Aims-To investigate the distribution and viral load of the most prevalent high risk human papillomavirus (HPV) types 16, 18, 31, 33, and 45 and low risk HPV types 6 and 11 in a variety of cervical lesions. Methods-One hundred and seventy six cytological specimens from women with diVerent cervical lesions were investigated. For an accurate standardisation of the sample, cervical cells were counted and a volume of the cell suspension processed by polymerase chain reactionenzyme linked immunosorbent assay (PCR-ELISA). Semiquantitative determinations were achieved in relation to an external reference titration curve. Results-HPV DNA was detected in 60.2% of the samples. HPV-16 was the prevalent genotype (57.6%), followed by HPV-33, HPV-31, HPV-6, HPV-18, and HPV-45. HPV-11 was not detected. HPV-16 showed a pronounced increase in prevalence with the evolution of cervical disease. Semiquantitative evaluation of the results showed that only HPV-16 DNA could reach very high values (> 1000 genome copies/cell) and a very high HPV-16 load correlated with the severity of cervical disease. Conclusions-Only HPV-16 load appears to be associated with the severity of cervical disease. (J Clin Pathol 2001;54:377-380) Keywords: human papillomavirus distribution; viral load; cervical lesions Cancer of the female genital tract is characterised by a long premalignant phase, and prevention of the disease has partially been achieved by cytological screening to identify premalignant lesions, which can be treated successfully. Epidemiological and molecular biological studies have shown a causal relation between human papillomavirus (HPV) infection and cervical neoplasia with high, intermediate or low oncogenic risk associated with different HPV genotypes. The association of cytological analysis with HPV detection and typing has significantly reduced the underestimation of histological alterations, and provides additional information for the follow up of patients with cytomorphologically abnormal cervical smears. [2][3][4] In addition, increased DNA loads of high risk HPVs in cervical specimens have been proposed as a specific marker for disease, as determined by hybrid capture assay, which discriminates between high and low risk HPVs, but cannot define the specific genotype.3 Semiquantitative determinations for type specific HPV DNA have also been achieved by type specific polymerase chain reaction (PCR) 5 For a correct interpretation of the results this study undertook a detailed standardisation of the sample: cervical cells were counted and a volume of the cell suspension was processed by PCR-enzyme linked immunosorbent assay (ELISA). 7 The assay was used to analyse the distribution and viral load of the most prevalent high risk HPV types 16, 18, 31, 33, and 45 and low risk HPV types 6 and 11 in 176 cytological specimens from immunocompetent Italian women with diVerent cervical lesions. Methods CLINICAL SPECIMENSA population of 176 Italian women with diVerent cervical lesions and without underlying immunological diseases w...

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