eThe association between human papillomavirus 31 (HPV31) DNA loads and the risk of cervical intraepithelial neoplasia grades 2 and 3 (CIN2-3) was evaluated among women enrolled in the atypical squamous cells of undetermined significance (ASCUS) and low-grade squamous intraepithelial lesion (LSIL) triage study (ALTS), who were monitored semiannually over 2 years and who had HPV31 infections detected at >1 visit. HPV31 DNA loads in the first HPV31-positive samples and in a random set of the last positive samples from women with >2 HPV31-positive visits were measured by a real-time PCR assay. CIN2-3 was histologically confirmed at the same time as the first detection of HPV31 for 88 (16.6%) of 530 women. After adjustment for HPV31 lineages, coinfection with other oncogenic types, and the timing of the first positive detection, the odds ratio (OR) per 1-log-unit increase in viral loads for the risk of a concurrent diagnosis of CIN2-3 was 1.5 (95% confidence interval [CI], 1.2 to 1.9). Of 373 women without CIN2-3 at the first positive visit who had >1 later visit, 44 had subsequent diagnoses of CIN2-3. The initial viral loads were associated with CIN2-3 diagnosed within 6 months after the first positive visit (adjusted OR, 1.5 [95% CI, 1.0 to 2.4]) but were unrelated to CIN2-3 diagnosed later. For a random set of 49 women who were tested for viral loads at the first and last positive visits, changes in viral loads were upward and downward among women with and without follow-up CIN2-3 diagnoses, respectively, although the difference was not statistically significant. Results suggest that HPV31 DNA load levels at the first positive visit signal a short-term but not long-term risk of CIN2-3. C ervical infection with oncogenic human papillomavirus (HPV) is a prerequisite for cervical cancer and its precursor lesions, which have typically been defined for clinical purposes as cervical intraepithelial neoplasia grades 2 and 3 (CIN2-3) (1). However, most infections are transient, with only a small proportion leading to the development of treatable cervical precancerous lesions (2, 3). It is still largely undetermined why, for a given type of HPV, some infections progress while others do not. The HPV DNA load, as measured in an exfoliated cervical scraping sample, reflects the number of free virions, the number of infected cells with either productive infection or clonal expansion, and the numbers of viral copies in individual cells. Whether HPV DNA load levels are associated with the risk of CIN2-3 deserves consideration.Studies of the clinical relevance of HPV DNA loads have focused mainly on HPV16 (4-8), the type that possesses the greatest oncogenic potential (9-11). Data on oncogenic types other than HPV16 are much less common. Some reports suggest that the viral-load-related risk of CIN2-3 may be HPV type specific (12, 13); others show that differences in slopes (daily changes in viral loads) between transient infections and infections leading to CIN3 are constant across types (14,15). HPV31 is one of the oncogenic typ...